Critical role of miR-21/exosomal miR-21 in autophagy pathway.

Activation of autophagy, a process of cellular stress response, leads to the breakdown of proteins, organelles, and other parts of the cell in lysosomes, and can be linked to several ailments, such as cancer, neurological diseases, and rare hereditary syndromes. Thus, its regulation is very carefully monitored. Transcriptional and post-translational mechanisms domestically or in whole organisms utilized to control the autophagic activity, have been heavily researched. In modern times, microRNAs (miRNAs) are being considered to have a part in post-translational orchestration of the autophagic activity, with miR-21 as one of the best studied miRNAs, it is often more than expressed in cancer cells. This regulatory RNA is thought to play a major role in a plethora of processes and illnesses including growth, cancer, cardiovascular disease, and inflammation. Different studies have suggested that a few autophagy-oriented genes, such as PTEN, Rab11a, Atg12, SIPA1L2, and ATG5, are all targeted by miR-21, indicating its essential role in the regulation.

Dietary polyphenols and the risk of metabolic syndrome: a systematic review and meta-analysis.

BACKGROUND: Accumulating evidence has suggested that dietary polyphenols may be protective against metabolic syndrome (MetS); however, the available evidence is contradictory. The aim of this meta-analysis was to assess the association between dietary intake of polyphenols and the odds of MetS. METHODS: The PubMed and Scopus databases were systematically searched to obtain eligible studies. The risk of MetS for the highest versus the lowest intakes of total, subclasses and individual polyphenols were examined by pooling odds ratios (OR) and 95% confidence intervals (95%CI) using the random effects model. RESULTS: A total of 14 studies (6 cohort and 8 cross-sectional studies) involving a total of 50,366 participants with 10,879 cases of MetS were included. When various polyphenol compounds were pooled, they were significantly related to a 22% decreased odds of MetS (([5 studies]; OR: 0.78; 95%CI: 0.72-0.85). Higher intakes of total flavonoids (([9 studies]; OR: 0.78; 95%CI: 0.72-0.85), flavan-3-ols (([2 studies]; OR: 0.64; 95%CI: 0.43-0.94), isoflavones (([3 studies]; OR: 0.84; 95%CI: 0.75-0.93), stilbenes (([4 studies]; OR: 0.86; 95%CI: 0.76-0.97), flavones (([2 studies]; OR: 0.79; 95%CI: 0.71-0.89), and quercetin (([2 studies]; OR: 0.63; 95%CI: 0.43-0.93) were also significantly associated with a decreased risk of MetS. The associations were not modified by the age of the participants. No association was found for total polyphenols, phenolic acids, lignans, anthocyanins, and flavonols. CONCLUSION: The results of this meta-analysis supported that higher polyphenol intake can lower the risk of MetS.

The Effects of Apigenin in the Treatment of Diabetic Nephropathy: A Systematic Review of Non-clinical Studies.

PURPOSE: Diabetes is one of the important and growing diseases in the world. Among the most common diabetic complications are renal adverse effects. The use of apigenin may prevent the development and progression of diabetes-related injuries. The current study aims to review the effects of apigenin in the treatment of diabetic nephropathy. METHODS: In this review, a systematic search was performed based on PRISMA guidelines for obtaining all relevant studies on "the effects of apigenin against diabetic nephropathy" in various electronic databases up to September 2022. Ninety-one articles were obtained and screened in accordance with the predefined inclusion and exclusion criteria. Seven eligible articles were finally included in this review. RESULTS: The experimental findings revealed that hyperglycemia led to the decreased cell viability of kidney cells and body weight loss and an increased kidney weight of rats; however, apigenin administration had a reverse effect on these evaluated parameters. It was also found that hyperglycemia could induce alterations in the biochemical and renal function-related parameters as well as histopathological injuries in kidney cells or tissue; in contrast, the apigenin administration could ameliorate the hyperglycemia-induced renal adverse effects. CONCLUSION: The results indicated that the use of apigenin could mitigate diabetes-induced renal adverse effects, mainly through its antioxidant, anti-apoptotic, and anti-inflammatory activities. Since the findings of this study are based on experimental studies, suggesting the use of apigenin (as a nephroprotective agent) against diabetic nephropathy requires further clinical studies.

Novel and potential therapy options for a range of cancer diseases: Using Flavonoid.

Cancer is a complex group of diseases characterized by the uncontrolled growth and spread of abnormal cells in the body. These abnormal cells can form tumors or invade nearby tissues and organs, leading to a range of health problems. There are many different types of cancer, which can be categorized based on the location of the primary tumor, the type of cell involved, and the stage of the disease. Some common types of cancer include breast cancer, lung cancer, colon cancer, prostate cancer, and skin cancer. Nanoparticles are very small particles, typically ranging in size from 1 to 100 nanometers, that have unique physical and chemical properties. These properties make them attractive for use in a variety of applications, including cancer treatment. Flavonoids, which are natural compounds found in fruits, vegetables, and other plant-based foods, have been extensively studied for their potential role in cancer prevention and treatment. Flavonoids have been shown to possess a wide range of biological activities, including antioxidant, anti-inflammatory, anti-cancer, and anti-metastatic effects.

Soluble receptor for advanced glycation end products (sRAGE) is associated with obesity rates: a systematic review and meta-analysis of cross-sectional study.

BACKGROUND: Several studies have highlighted the possible positive effects of soluble receptor for advanced glycation end products (sRAGE) against obesity. However, due to their inconsistent results, this systematic review and meta-analysis aimed to quantitatively evaluate and critically review the results of studies evaluating the relationship between sRAGE with obesity among adult population. METHODS: In the systematic search, the eligibility criteria were as follows: studies conducted with a cross-sectional design, included apparently healthy adults, adults with obesity, or obesity-related disorders, aged over 18 years, and evaluated the association between general or central obesity indices with sRAGE. RESULTS: Our systematic search in electronic databases, including PubMed, Scopus, and Embase up to 26 October, 2023 yielded a total of 21,612 articles. After removing duplicates, screening the titles and abstracts, and reading the full texts, 13 manuscripts were included in the final meta-analysis. According to our results, those at the highest category of circulating sRAGE concentration with median values of 934.92 pg/ml of sRAGE, had 1.9 kg/m2 lower body mass index (BMI) (WMD: -1.927; CI: -2.868, -0.986; P < 0.001) compared with those at the lowest category of sRAGE concentration with median values of 481.88 pg/ml. Also, being at the highest sRAGE category with the median values of 1302.3 pg/ml sRAGE, was accompanied with near 6 cm lower waist circumference (WC) (WMD: -5.602; CI: -8.820, -2.383; P < 0.001 with 86.4% heterogeneity of I2) compared with those at the lowest category of sRAGE concentration with median values of 500.525 pg/ml. Individuals with obesity had significantly lower circulating sRAGE concentrations (WMD: -135.105; CI: -256.491, -13.72; P = 0.029; with 79.5% heterogeneity of I2). According to the subgrouping and meta-regression results, country and baseline BMI were possible heterogeneity sources. According to Begg's and Egger's tests and funnel plots results, there was no publication bias. CONCLUSION: According to our results, higher circulating sRAGE concentrations was associated with lower BMI and WC among apparently healthy adults. Further randomized clinical trials are warranted for possible identification of causal associations.

Melatonin in Chemo/Radiation Therapy; Implications for Normal Tissues Sparing and Tumor Suppression: An Updated Review.

Resistance to therapy and the toxicity of normal tissue are the major problems for efficacy associated with chemotherapy and radiotherapy. Drug resistance is responsible for most cases of mortality associated with cancer. Furthermore, their side effects can decrease the quality of life for surviving patients. An enhancement in the tumor response to therapy and alleviation of toxic effects remain unsolved challenges. One of the interesting topics is the administration of agents with low toxicity to protect normal tissues and/or sensitize cancers to chemo/radiotherapy. Melatonin is a natural body hormone that is known as a multitasking molecule. Although it has antioxidant properties, a large number of experiments have uncovered interesting effects of melatonin that can increase the therapeutic efficacy of chemo/radiation therapy. Melatonin can enhance anticancer therapy efficacy through various mechanisms, cells such as the immune system, and modulation of cell cycle and death pathways, tumor suppressor genes, and also through suppression of some drug resistance mediators. However, melatonin may protect normal tissues through the suppression of inflammation, fibrosis, and massive oxidative stress in normal cells and tissues. In this review, we will discuss the distinct effects of melatonin on both tumors and normal tissues. We review how melatonin may enhance radio/chemosensitivity of tumors while protecting normal tissues such as the lung, heart, gastrointestinal system, reproductive system, brain, liver, and kidney.

The Radiosensitizing Potentials of Silymarin/Silibinin in Cancer: A Systematic Review.

INTRODUCTION: Although radiotherapy is one of the main cancer treatment modalities, exposing healthy organs/tissues to ionizing radiation during treatment and tumor resistance to ionizing radiation are the chief challenges of radiotherapy that can lead to different adverse effects. It was shown that the combined treatment of radiotherapy and natural bioactive compounds (such as silymarin/silibinin) can alleviate the ionizing radiation-induced adverse side effects and induce synergies between these therapeutic modalities. In the present review, the potential radiosensitization effects of silymarin/silibinin during cancer radiation exposure/radiotherapy were studied. METHODS: According to the PRISMA guideline, a systematic search was performed for the identification of relevant studies in different electronic databases of Google Scholar, PubMed, Web of Science, and Scopus up to October 2022. We screened 843 articles in accordance with a predefined set of inclusion and exclusion criteria. Seven studies were finally included in this systematic review. RESULTS: Compared to the control group, the cell survival/proliferation of cancer cells treated with ionizing radiation was considerably less, and silymarin/silibinin administration synergistically increased ionizing radiation-induced cytotoxicity. Furthermore, there was a decrease in the tumor volume, weight, and growth of ionizing radiation-treated mice as compared to the untreated groups, and these diminutions were predominant in those treated with radiotherapy plus silymarin/ silibinin. Furthermore, the irradiation led to a set of biochemical and histopathological changes in tumoral cells/tissues, and the ionizing radiation-induced alterations were synergized following silymarin/silibinin administration (in most cases). CONCLUSION: In most cases, silymarin/silibinin administration could sensitize the cancer cells to ionizing radiation through an increase of free radical formation, induction of DNA damage, increase of apoptosis, inhibition of angiogenesis and metastasis, etc. However, suggesting the use of silymarin/silibinin during radiotherapeutic treatment of cancer patients requires further clinical studies.

Dietary caffeine intake is associated with favorable metabolic profile among apparently healthy overweight and obese individuals.

BACKGROUND: Recent studies have revealed some conflicting results about the health effects of caffeine. These studies are inconsistent in terms of design and population and source of consumed caffeine. In the current study, we aimed to evaluate the possible health effects of dietary caffeine intake among overweight and obese individuals. METHODS: In this cross-sectional study, 488 apparently healthy individuals with overweight and obesity were participated. Dietary intake was assessed by a Food Frequency Questionnaire (FFQ) and the amount of dietary caffeine was calculated. Body composition was determined by bioelectrical impedance analysis (BIA). Enzymatic methods were used to evaluate serum lipid, glucose, and insulin concentrations. RESULTS: Those at the highest tertile of dietary caffeine intake had lower percentage of fat mass, higher fat free mass and appetite score (P < 0.05). Also, lower total cholesterol (TC) and low density lipoprotein cholesterol (LDL-c) was observed in higher tertiles of dietary caffeine intake compared with lower tertiles. In multinomial adjusted models, those at the second tertile of dietary caffeine intake were more likely to have higher serum insulin (P = 0.04) and lower homeostatic model assessment of insulin resistance (HOMA-IR) values compared with first tertile (P = 0.03) in crude model. While, in the age, body mass index (BMI), sex, physical activity, socio-economic status (SES) and energy intake -adjusted model (Model III), those at the third tertile of dietary caffeine intake were more likely to have low serum LDL concentrations [odds ratio (OR) = 0.957; CI = 0.918-0.997; P = 0.04]. With further adjustment to dietary vegetable, fiber and grain intake, those at the third tertile of dietary caffeine intake were more likely to have low systolic blood pressure (SBP), LDL and high HDL levels compared with those at the first tertile (P < 0.05). CONCLUSION: High intakes of dietary caffeine was associated with lower LDL, SBP, insulin resistance and higher HDL concentrations among overweight and obese individuals. However, due to observational design of the study, causal inference is impossible and further studies are warranted to confirm our findings.

Functions of LncRNAs, exosomes derived MSCs and immune regulatory molecules in preeclampsia disease.

Modulatory signaling pathway such as T cell immunoreceptor with Ig and ITIM domains (TIGIT), Cytotoxic T-Lymphocyte Associated Protein 4 (CTLA-4), P53 signaling and TIM (T-cell immunoglobin and mucin domain) are important in normal pregnancy and loss of their functions or dysregulation of related genes can lead to some disorders. Inflammation is a process by which your body's white blood cells and the things they make protect you from infection from outside invaders, such as bacteria and viruses. Some cellular and molecular signaling have been categorized to demonstrate the mechanism that protects tolerance to antigens. lncRNAs significantly impact physiological processes like immunity and metabolism, and are linked to tumors, cardiovascular diseases, nervous system disorders, and nephropathy.In this review article, we summarized recent studies about the role of TIGIT, CTLA-4, P53 and TIM regulatory molecules and reviewed dysregulation of these pathway in diseases.We will also talk about the role of lncRNAs and mesenchymal stem cells.

A state-of-art of underlying molecular mechanisms and pharmacological interventions/nanotherapeutics for cisplatin resistance in gastric cancer.

The fourth common reason of death among patients is gastric cancer (GC) and it is a dominant tumor type in Ease Asia. One of the problems in GC therapy is chemoresistance. Cisplatin (CP) is a platinum compound that causes DNA damage in reducing tumor progression and viability of cancer cells. However, due to hyperactivation of drug efflux pumps, dysregulation of genes and interactions in tumor microenvironment, tumor cells can develop resistance to CP chemotherapy. The current review focuses on the CP resistance emergence in GC cells with emphasizing on molecular pathways, pharmacological compounds for reversing chemoresistance and the role of nanostructures. Changes in cell death mechanisms such as upregulation of pro-survival autophagy can prevent CP-mediated apoptosis that results in drug resistance. Moreover, increase in metastasis via EMT induction induces CP resistance. Dysregulation of molecular pathways such as PTEN, PI3K/Akt, Nrf2 and others result in changes in CP response of GC cells. Non-coding RNAs determine CP response of GC cells and application of pharmacological compounds with activity distinct of CP can result in sensitivity in tumor cells. Due to efficacy of exosomes in transferring bioactive molecules such as RNA and DNA molecules among GC cells, exosomes can also result in CP resistance. One of the newest progresses in overcoming CP resistance in GC is application of nanoplatforms for delivery of CP in GC therapy that they can increase accumulation of CP at tumor site and by suppressing carcinogenic factors and overcoming biological barriers, they increase CP toxicity on cancer cells.

LncRNA PVT1: as a therapeutic target for breast cancer.

A significant number of women are identified with breast cancer (BC) every year, making it among the most prevalent malignancies and one of the leading causes of mortality globally. Despite significant progress in understanding BC pathogenesis and treatment options, there is still a need to identify new therapeutic targets and develop more effective treatments. LncRNAs have been discovered as biomarkers and a promising target for various cancers, including BC. PVT1 is a particular one of these lncRNAs, and research has indicated that it has a significant impact on the appearance and progression of BC.PVT1 is an attractive therapeutic target for BC due to its role in promoting cancer cell growth, metastasis and invasion. In addition to its potential as a treatment strategy, PVT1 may also have diagnostic value in BC. In this article, we will discuss targeting PVT1 as a treatment strategy for BC.

The metformin immunoregulatory actions in tumor suppression and normal tissues protection.

The immune system is the key player in a wide range of responses in normal tissues and tumors to anticancer therapy. Inflammatory and fibrotic responses in normal tissues are the main limitations of chemotherapy, radiotherapy, and also some newer anticancer drugs such as immune checkpoint inhibitors (ICIs). Immune system responses within solid tumors including anti-tumor and tumor-promoting responses can suppress or help tumor growth. Thus, modulation of immune cells and their secretions such as cytokines, growth factors and epigenetic modulators, pro-apoptosis molecules, and some other molecules can be suggested to alleviate side effects in normal tissues and drug-resistance mechanisms in the tumor. Metformin as an anti-diabetes drug has shown intriguing properties such as anti-inflammation, anti-fibrosis, and anticancer effects. Some investigations have uncovered that metformin can ameliorate radiation/chemotherapy toxicity in normal cells and tissues through the modulation of several targets in cells and tissues. These effects of metformin may ameliorate severe inflammatory responses and fibrosis after exposure to ionizing radiation or following treatment with highly toxic chemotherapy drugs. Metformin can suppress the activity of immunosuppressive cells in the tumor through the phosphorylation of AMP-activated protein kinase (AMPK). In addition, metformin may stimulate antigen presentation and maturation of anticancer immune cells, which lead to the induction of anticancer immunity in the tumor. This review aims to explain the detailed mechanisms of normal tissue sparing and tumor suppression during cancer therapy using adjuvant metformin with an emphasis on immune system responses.

Angiogenesis and prostate cancer: MicroRNAs comes into view.

Angiogenesis, the formation of new blood vessels, is an important stage in the growth of cancer. Extracellular matrix, endothelial cells, and soluble substances must be carefully coordinated during the multistep procedure of angiogenesis. Inducers and inhibitors have been found to control pretty much every phase. In addition to benign prostatic hyperplasia, prostatic intraepithelial neoplasia, and angiogenesis have a critical role in the initiation and progression of prostate cancer. MicroRNA (miRNA) is endogenous, short, non-coding RNA molecules of almost 22 nucleotides play a role in regulating cellular processes and regulating several genes' expression. Through controlling endothelial migration, differentiation, death, and cell proliferation, miRNAs have a significant function in angiogenesis. A number of pathological and physiological processes, particularly prostate cancer's emergence, depend on the regulation of angiogenesis. Investigating the functions played with miRNAs in angiogenesis is crucial because it might result in the creation of novel prostate cancer therapies that entail regulating angiogenesis. The function of several miRNAs and its targeting genes engaged in cancer of the prostate angiogenesis will be reviewed in this review in light of the most recent developments. The potential clinical utility of miRNAs potentially a novel therapeutic targets will also be explored, as well as their capacity to control prostate cancer angiogenesis and the underlying mechanisms.

The interactions of docetaxel with tumor microenvironment.

There are several interactions within the tumor microenvironment (TME) that affect the response of cancer cells to therapy. There are also a large number of cells and secretions in TME that increase resistance to therapy. Following the release of immunosuppressive, pro-angiogenic, and metastatic molecules by certain cells such as tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), and cancer cells, immune evasion, angiogenesis, and metastasis may be induced. However, natural killer (NK) cells and cytotoxic CD8 + T lymphocytes (CTLs) can responsively release anticancer molecules. In addition, anticancer drugs can modulate these cells and their interactions in favor of either cancer resistance or therapy. Docetaxel belongs to taxanes, a class of anti-tumor drugs, which acts through the polymerization of tubulin and the induction of cell cycle arrest. Also, it has been revealed that taxanes including docetaxel affect cancer cells and the other cells within TME through some other mechanisms such as modulation of immune system responses, angiogenesis, and metastasis. In this paper, we explain the basic mechanisms of docetaxel interactions with malignant cells. Besides, we review the diverse effects of docetaxel on TME and cancer cells in consequence. Lastly, the modulatory effects of docetaxel alone or in conjunction with other anticancer agents on anti-tumor immunity, cancer cell resistance, angiogenesis, and metastasis will be discussed.

The key role of microRNA-766 in the cancer development.

Cancer is caused by defects in coding and non-coding RNAs. In addition, duplicated biological pathways diminish the efficacy of mono target cancer drugs. MicroRNAs (miRNAs) are short, endogenous, non-coding RNAs that regulate many target genes and play a crucial role in physiological processes such as cell division, differentiation, cell cycle, proliferation, and apoptosis, which are frequently disrupted in diseases such as cancer. MiR-766, one of the most adaptable and highly conserved microRNAs, is notably overexpressed in several diseases, including malignant tumors. Variations in miR-766 expression are linked to various pathological and physiological processes. Additionally, miR-766 promotes therapeutic resistance pathways in various types of tumors. Here, we present and discuss evidence implicating miR-766 in the development of cancer and treatment resistance. In addition, we discuss the potential applications of miR-766 as a therapeutic cancer target, diagnostic biomarker, and prognostic indicator. This may shed light on the development of novel therapeutic strategies for cancer therapy.

Prostate cancer and microRNAs: New insights into apoptosis.

Prostate cancer (PCa) is known as one of the most prevalent malignancies globally and is not yet curable owing to its progressive nature. It has been well documented that Genetic and epigenetic alterations maintain mandatory roles in PCa development. Apoptosis, a form of programmed cell death, has been shown to be involved in a number of physiological processes. Apoptosis disruption is considered as one of the main mechanism involved in lots of pathological conditions, especially malignancy. There is ample of evidence in support of the fact that microRNAs (miRNAs) have crucial roles in several cellular biological processes, including apoptosis. Escaping from apoptosis is a common event in malignancy progression. Emerging evidence revealed miRNAs capabilities to act as apoptotic or anti-apoptotic factors by altering the expression levels of tumor inhibitor or oncogene genes. In the present narrative review, we described in detail how apoptosis dysfunction could be involved in PCa processes and additionally, the mechanisms behind miRNAs affect the apoptosis pathways in PCa. Identifying the mechanisms behind the effects of miRNAs and their targets on apoptosis can provide scientists new targets for PCa treatment.

Nanotechnology-empowered lung cancer therapy: From EMT role in cancer metastasis to application of nanoengineered structures for modulating growth and metastasis.

Lung cancer is one of the leading causes of death in both males and females, and it is the first causes of cancer-related deaths. Chemotherapy, surgery and radiotherapy are conventional treatment of lung cancer and recently, immunotherapy has been also appeared as another therapeutic strategy for lung tumor. However, since previous treatments have not been successful in cancer therapy and improving prognosis and survival rate of lung tumor patients, new studies have focused on gene therapy and targeting underlying molecular pathways involved in lung cancer progression. Nanoparticles have been emerged in treatment of lung cancer that can mediate targeted delivery of drugs and genes. Nanoparticles protect drugs and genes against unexpected interactions in blood circulation and improve their circulation time. Nanoparticles can induce phototherapy in lung cancer ablation and mediating cell death. Nanoparticles can induce photothermal and photodynamic therapy in lung cancer. The nanostructures can impair metastasis of lung cancer and suppress EMT in improving drug sensitivity. Metastasis is one of the drawbacks observed in lung cancer that promotes migration of tumor cells and allows them to establish new colony in secondary site. EMT can occur in lung cancer and promotes tumor invasion. EMT is not certain to lung cancer and it can be observed in other human cancers, but since lung cancer has highest incidence rate, understanding EMT function in lung cancer is beneficial in improving prognosis of patients. EMT induction in lung cancer promotes tumor invasion and it can also lead to drug resistance and radio-resistance. Moreover, non-coding RNAs and pharmacological compounds can regulate EMT in lung cancer and EMT-TFs such as Twist and Slug are important modulators of lung cancer invasion that are discussed in current review.

Multifaceted role of NF-κB in hepatocellular carcinoma therapy: Molecular landscape, therapeutic compounds and nanomaterial approaches.

The predominant kind of liver cancer is hepatocellular carcinoma (HCC) that its treatment have been troublesome difficulties for physicians due to aggressive behavior of tumor cells in proliferation and metastasis. Moreover, stemness of HCC cells can result in tumor recurrence and angiogenesis occurs. Another problem is development of resistance to chemotherapy and radiotherapy in HCC cells. Genomic mutations participate in malignant behavior of HCC and nuclear factor-kappaB (NF-κB) has been one of the oncogenic factors in different human cancers that after nuclear translocation, it binds to promoter of genes in regulating their expression. Overexpression of NF-κB has been well-documented in increasing proliferation and invasion of tumor cells and notably, when its expression enhances, it induces chemoresistance and radio-resistance. Highlighting function of NF-κB in HCC can shed some light on the pathways regulating progression of tumor cells. The first aspect is proliferation acceleration and apoptosis inhibition in HCC cells mediated by enhancement in expression level of NF-κB. Moreover, NF-κB is able to enhance invasion of HCC cells via upregulation of MMPs and EMT, and it triggers angiogenesis as another step for increasing spread of tumor cells in tissues and organs. When NF-κB expression enhances, it stimulates chemoresistance and radio-resistance in HCC cells and by increasing stemness and population of cancer-stem cells, it can provide the way for recurrence of tumor. Overexpression of NF-κB mediates therapy resistance in HCC cells and it can be regulated by non-coding RNAs in HCC. Moreover, inhibition of NF-κB by anti-cancer and epigenetic drugs suppresses HCC tumorigenesis. More importantly, nanoparticles are considered for suppressing NF-κB axis in cancer and their prospectives and results can also be utilized for treatment of HCC. Nanomaterials are promising factors in treatment of HCC and by delivery of genes and drugs, they suppress HCC progression. Furthermore, nanomaterials provide phototherapy in HCC ablation.

Harnessing function of EMT in hepatocellular carcinoma: From biological view to nanotechnological standpoint.

Management of cancer metastasis has been associated with remarkable reduction in progression of cancer cells and improving survival rate of patients. Since 90% of mortality are due to cancer metastasis, its suppression can improve ability in cancer fighting. The EMT has been an underlying cause in increasing cancer migration and it is followed by mesenchymal transformation of epithelial cells. HCC is the predominant kind of liver tumor threatening life of many people around the world with poor prognosis. Increasing patient prognosis can be obtained via inhibiting tumor metastasis. HCC metastasis modulation by EMT and HCC therapy by nanoparticles are discussed here. First of all, EMT happens during progression and advanced stages of HCC and therefore, its inhibition can reduce tumor malignancy. Moreover, anti-cancer compounds including all-trans retinoic acid and plumbaging, among others, have been considered as inhibitors of EMT. The EMT association with chemoresistance has been evaluated. Moreover, ZEB1/2, TGF-ß, Snail and Twist are EMT modulators in HCC and enhancing cancer invasion. Therefore, EMT mechanism and related molecular mechanisms in HCC are evaluated. The treatment of HCC has not been only emphasized on targeting molecular pathways with pharmacological compounds and since drugs have low bioavailability, their targeted delivery by nanoparticles promotes HCC elimination. Moreover, nanoparticle-mediated phototherapy impairs tumorigenesis in HCC by triggering cell death. Metastasis of HCC and even EMT mechanism can be suppressed by cargo-loaded nanoparticles.

The association between prenatal exposure to polycyclic aromatic hydrocarbons and childhood intelligence: a systematic review of observational studies.

Exposure to polycyclic aromatic hydrocarbons (PAHs) during pregnancy has been associated with many adverse child health. However, the evidence on such associations with child brain development was not reviewed systemically. Therefore, in this study, we systemically reviewed the observational studies on prenatal exposure to PAHs and childhood intelligence quotient (IQ). The Meta-analyses Of Observational Studies in Epidemiology (MOOSE) guidelines were applied to perform this review. We systematically searched Scopus, PubMed, and Web of Science for all relevant articles published in English until 15 October 2022. The quality of retrieved studies was evaluated based on the Gascon et al. method. We retrieved a total of 351 citations through the initial search, of which an overall of six articles ([Formula: see text] participants) were included in our final review. The quality assessment indicated that four studies had excellent and two studies had good quality. Three reviewed studies reported a significant negative association between prenatal exposure to PAHs and children's IQ. One study reported that exposure to PAHs combined with material hardship was associated with lower child IQ and one study indicated lower child IQ through lower LINE1 DNA methylation-related maternal exposure to PAHs. However, another study did not observe a significant association between prenatal PAH exposure and child IQ. Overall, our review indicated that exposure to PAHs during pregnancy has an adverse impact on childhood IQ.