The impact of curcumin on migraine: A comprehensive review.

Migraine, a neurovascular condition, is a chronic and lifelong disease that affects about 15% of the population worldwide. Although the exact pathophysiology and etiology of migraine are still unclear, oxidative stress, inflammation, and neuroendocrine imbalances are identified as the critical risk factors for migraine attacks. Curcumin is an active component and a polyphenolic diketone compound extracted from turmeric. Curcumin is a promising candidate for preventing and controlling migraine due to its anti­inflammatory, antioxidative, anti-protein aggregate, and analgesic effects. In the present review, we have evaluated experimental and clinical studies investigating the impact of liposomal curcumin and nano-curcumin on the frequency and severity of migraine attacks in patients. Although the results are promising, more studies should be conducted in this area to show the exact efficacies of curcumin on clinical symptoms of migraine and investigate its potential mechanisms.

Long non-coding RNAs (lncRNAs) in hepatocellular carcinoma progression: Biological functions and new therapeutic targets.

Liver is an important organ in body that performs vital functions such as detoxification. Liver is susceptible to development of cancers, and hepatocellular carcinoma (HCC) is among them. 75-85% of liver cancer cases are related to HCC. Therefore, much attention has been directed towards understanding factors mediating HCC progression. LncRNAs are epigenetic factors with more than 200 nucleotides in length located in both nucleus and cytoplasm and they are promising candidates in cancer therapy. Directing studies towards understanding function of lncRNAs in HCC is of importance. LncRNAs regulate cell cycle progression and growth of HCC cells, and they can also induce/inhibit apoptosis in tumor cells. LncRNAs affect invasion and metastasis in HCC mainly by epithelial-mesenchymal transition (EMT) mechanism. Revealing the association between lncRNAs and downstream signaling pathways in HCC is discussed in the current manuscript. Infectious diseases can affect lncRNA expression in mediating HCC development and then, altered expression level of lncRNA is associated with drug resistance and radio-resistance. Biomarker application of lncRNAs and their role in prognosis and diagnosis of HCC are also discussed to pave the way for treatment of HCC patients.

Climate Stressors and Physiological Dysregulations: Mechanistic Connections to Pathologies.

This review delves into the complex relationship between environmental factors, their mechanistic cellular and molecular effects, and their significant impact on human health. Climate change is fueled by industrialization and the emission of greenhouse gases and leads to a range of effects, such as the redistribution of disease vectors, higher risks of disease transmission, and shifts in disease patterns. Rising temperatures pose risks to both food supplies and respiratory health. The hypothesis addressed is that environmental stressors including a spectrum of chemical and pathogen exposures as well as physical and psychological influences collectively impact genetics, metabolism, and cellular functions affecting physical and mental health. The objective is to report the mechanistic associations linking environment and health. As environmental stressors intensify, a surge in health conditions, spanning from allergies to neurodegenerative diseases, becomes evident; however, linkage to genetic-altered proteomics is more hidden. Investigations positing that environmental stressors cause mitochondrial dysfunction, metabolic syndrome, and oxidative stress, which affect missense variants and neuro- and immuno-disorders, are reported. These disruptions to homeostasis with dyslipidemia and misfolded and aggregated proteins increase susceptibility to cancers, infections, and autoimmune diseases. Proposed interventions, such as vitamin B supplements and antioxidants, target oxidative stress and may aid mitochondrial respiration and immune balance. The mechanistic interconnections of environmental stressors and disruptions in health need to be unraveled to develop strategies to protect public health.

A meta-analysis of effects of vitamin E supplementation alone and in combination with omega-3 or magnesium on polycystic ovary syndrome.

Vitamin E supplementation might have favorable effects on risk factors of polycystic ovary syndrome (PCOS). This systematic review and meta-analysis aimed to summarize the effects of vitamin E supplementation or vitamin E in combination with omega-3 or magnesium on PCOS. PubMed, Scopus, ISI Web of Science, Cochrane, Embase electronic databases, and Google scholar were searched for all available articles up to September 2022. Randomized controlled trials (RCTs) that examined the effect of vitamin E supplementation or vitamin E in combination with omega-3 or magnesium on lipid and glycemic profiles, anthropometric measurements, biomarkers of inflammation and oxidative stress, hormonal profile, and hirsutism score in patients with PCOS were included. Ten RCTs (with 504 participants) fulfilled the eligible criteria. Vitamin E supplementation or vitamin E in combination with omega-3 or magnesium in comparison to placebo could significantly reduce serum levels of TG (weighted mean difference: - 18.27 mg/dL, 95% CI - 34.68 to - 1.87), VLDL (- 5.88 mg/dL, 95% CI - 8.08 to - 3.68), LDL-c (- 12.84 mg/dL, 95% CI - 22.15 to - 3.52), TC (- 16.30 mg/dL, 95% CI - 29.74 to - 2.86), TC/HDL-c ratio (- 0.52, 95% CI - 0.87 to - 0.18), hs-CRP (- 0.60 ng/mL, 95% CI - 0.77 to - 0.44), hirsutism score (- 0.33, 95% CI - 0.65 to - 0.02) and significantly increase nitric oxide levels (2.79 µmol/L, 95% CI 0.79-4.79). No significant effect was found on HDL-c, glycemic indices, hormonal profile, anthropometric measurements, and other biomarkers of inflammation or oxidative stress. This meta-analysis highlights the potential anti-hyperlipidemic, anti-oxidant, and anti-inflammatory properties of vitamin E supplementation alone or in combination with omega-3 or magnesium on PCOS patients.

Crosstalk of miRNAs with signaling networks in bladder cancer progression: Therapeutic, diagnostic and prognostic functions.

Urological cancers are considered as life-threatening diseases around the world. Bladder cancer is one of the most malignant urological tumors with high mortality and morbidity. Bladder cancer is a heterogenous disease and genetic alterations have shown to be key players in regulating its progression. Although conventional therapies are somewhat beneficial in improving prognosis and survival, bladder cancer patients suffer from recurrence. MicroRNAs (miRNAs) are endogenous short RNA molecules that do not encode proteins and show dysregulated expression in human cancers. miRNAs are regulators of vital biological processes in cells such as proliferation, migration, differentiation and apoptosis. Dysregulation of miRNAs is observed in bladder cancer and they are used as biomarkers for diagnosis and prognosis of patients. LncRNAs and circRNAs are modulators of bladder cancer progression via miRNA expression regulation. Overexpression of onco-suppressor miRNAs impairs bladder cancer progression, while oncogenic miRNAs drive tumor progression. Glycolysis and EMT mechanisms are two important factors for proliferation and migration of bladder cancer that are modulated by miRNAs. Furthermore, miRNAs can affect STAT3 and Wnt/ß-catenin as instances of molecular factors in regulating bladder tumor progression. Bladder tumor response to drug therapy and radiotherapy is regulated by miRNAs. Hence, aim of current review is to provide function of miRNAs in bladder cancer based on their crosstalk with other molecular pathways and interaction with biological processes.

EMT mechanism in breast cancer metastasis and drug resistance: Revisiting molecular interactions and biological functions.

One of the malignant tumors in women that has involved both developed and developing countries is breast cancer. Similar to other types of tumors, breast cancer cells demonstrate high metastatic nature. Besides, breast tumor cells have ability of developing drug resistance. EMT is the related mechanism to cancer metastasis and focus of current manuscript is highlighting function of EMT in breast tumor malignancy and drug resistance. Breast tumor cells increase their migration by EMT induction During EMT, N-cadherin and vimentin levels increase, and E-cadherin levels decrease to mediate EMT-induced breast tumor invasion. Different kinds of anti-cancer agents such as tamoxifen, cisplatin and paclitaxel that EMT induction mediates chemoresistance feature of breast tumor cells. Furthermore, EMT induction correlates with radio-resistance in breast tumor. Clinical aspect is reversing EMT in preventing chemotherapy or radiotherapy failure in breast cancer patients and improving their survival time. The anti-tumor agents that suppress EMT can be used for decreasing breast cancer invasion and increasing chemosensitivity of tumor cells. Furthermore, lncRNAs, miRNAs and other factors can modulate EMT in breast tumor progression that are discussed here.

SOX2 function in cancers: Association with growth, invasion, stemness and therapy response.

Cancer is a leading cause of death worldwide and around 10 million deaths in 2020 were related to cancer. There are a number of therapeutic modalities for cancer such as chemotherapy, radiotherapy and surgery. However, tumor cells have capacity of developing resistance to chemotherapy and radiotherapy. Genetic mutations participate in development and progression of cancer. The current review focuses on the role of SOX2 transcription factor in cancer. SOX2 has capacity of increasing growth and metastasis of cancer cells. It functions as double-edged sword and has ability of suppressing tumor progression. Increasing evidence reveals that SOX2 is involved in triggering resistance to chemotherapy and radiotherapy. SOX2 promotes stemness of tumor cells and increases the number of cancer stem cells. SOX2 overexpression occurs in the tumor cells and tissues to ensure their proliferation and metastasis. Silencing SOX2 using CRISPR or siRNA impairs progression of the cancer cells and reduces their survival rate. SOX2 demonstrates interactions with other factors such as miRNAs, lncRNAs, STAT3 and Wnt/ß-catenin, among others to regulate progression of the tumor cells. SOX2 can be considered as a biomarker in cancer patients. SOX2 overexpression is associated with lymph node metastasis, low survival rate and poor prognosis of cancer patients.

LncRNA-miRNA axis in tumor progression and therapy response: An emphasis on molecular interactions and therapeutic interventions.

Epigenetic factors are critical regulators of biological and pathological mechanisms and they could interact with different molecular pathways. Targeting epigenetic factors has been an idea approach in disease therapy, especially cancer. Accumulating evidence has highlighted function of long non-coding RNAs (lncRNAs) as epigenetic factors in cancer initiation and development and has focused on their association with downstream targets. microRNAs (miRNAs) are the most well-known targets of lncRNAs and present review focuses on lncRNA-miRNA axis in malignancy and therapy resistance of tumors. LncRNA-miRNA regulates cell death mechanisms such as apoptosis and autophagy in cancers. This axis affects tumor metastasis via regulating EMT and MMPs. Besides, lncRNA-miRNA axis determines sensitivity of tumor cells to chemotherapy, radiotherapy and immunotherapy. Based on the studies, lncRNAs can be affected by drugs and genetic tools in cancer therapy and this may affect expression level of miRNAs as their downstream targets, leading to cancer suppression/progression. LncRNAs have both tumor-promoting and tumor-suppressor functions in cancer and this unique function of lncRNAs has complicated their implication in tumor therapy. LncRNA-miRNA axis can also affect other signaling networks in cancer such as PI3K/Akt, STAT3, Wnt/ß-catenin and EZH2 among others. Notably, lncRNA/miRNA axis can be considered as a signature for diagnosis and prognosis in cancers.

PLA1A expression as a diagnostic marker of BRAF-mutant metastasis in melanoma cancer.

BRAF and NRAS are the most reported mutations associated to melanomagenesis. The lack of accurate diagnostic markers in response to therapeutic treatment in BRAF/NRAS-driven melanomagenesis is one of the main challenges in melanoma personalized therapy. In order to assess the diagnostic value of phosphatidylserine-specific phospholipase A1-alpha (PLA1A), a potent lysophospholipid mediating the production of lysophosphatidylserine, PLA1A mRNA and serum levels were compared in subjects with malignant melanoma (n = 18), primary melanoma (n = 13), and healthy subjects (n = 10). Additionally, the correlation between histopathological subtypes of BRAF/NRAS-mutated melanoma and PLA1A was analyzed. PLA1A expression was significantly increased during melanogenesis and positively correlated to disease severity and histopathological markers of metastatic melanoma. PLA1A mRNA and serum levels were significantly higher in patients with BRAF-mutated melanoma compared to the patients with NRAS-mutated melanoma. Notably, PLA1A can be used as a diagnostic marker for an efficient discrimination between naïve melanoma samples and advanced melanoma samples (sensitivity 91%, specificity 57%, and AUC 0.99), as well as BRAF-mutated melanoma samples (sensitivity 62%, specificity 61%, and AUC 0.75). Our findings suggest that PLA1A can be considered as a potential diagnostic marker for advanced and BRAF-mutated melanoma.

Vitamin D Supplementation for Premenstrual Syndrome-Related inflammation and antioxidant markers in students with vitamin D deficient: a randomized clinical trial.

Premenstrual syndrome (PMS) is a common disorder in the reproductive age that negatively significant impacts on women's quality of life. This randomized clinical trial study was undertaken to investigate the effect of vitamin D supplementation on inflammatory and antioxidant markers in 44 vitamin D deficient (25(OH)D < 20 ng/mL) students with PMS. Participants received either 50,000 IU vitamin D3 or a placebo pearl fortnightly for 4 months. At the baseline and in the last 2 months of intervention, participants were asked to complete the PMS Daily Symptoms Rating form along with taking the pearls and their blood samples were collected to assess serum levels of 25(OH)D3, Interleukin10 and 12 (IL-10, IL-12) and total antioxidant capacity (TAC). In vitamin D group, serum levels of IL-10 and IL-12 significantly decreased while TAC significantly increased post-intervention. There were significant differences regarding serum IL-12 and TAC levels between the two groups. Mean score of the total PMS symptoms showed significant improvement in 25(OH)D. Vitamin D supplementation seems to be an effective strategy to improve inflammation and antioxidant markers in vitamin D deficient women with PMS. This clinical trial was registered at Iranian Registry of Clinical Trials on 20/06/2018 (IRCT20180525039822N1).