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Since suppressor/enhancer of Lin-12-like (SEL1L) was cloned in 1997, various pieces of evidence from lower species suggest it plays a significant role in protein degradation via the ubiquitin-proteasome system. The relevance of SEL1L in many aspects of malignant transformation and tumorigenic events has been the subject of research, which has shown compelling in vitro and in vivo findings relating its altered expression to changes in tumor aggressiveness. The Endoplasmic Reticulum (ER) in tumor cells is crucial for preserving cellular proteostasis by inducing the unfolded protein response (UPR), a stress response. A crucial component of the UPR is ER-associated degradation (ERAD), which guards against ER stress-induced apoptosis and the removal of unfolded or misfolded proteins by the ubiquitin-proteasome system. As a protein stabilizer of HMG-CoA reductase degradation protein 1 (HRD1), one of the main components of ERAD, SEL1L plays an important role in ER homeostasis. Notably, the expression levels of these two proteins fluctuate independently in various cancer types, yet changes in their expression affect the levels of other associated proteins during cancer pathogenesis. Recent studies have also outlined the function of SEL1L in cancer medication resistance. This review explores the value of targeting SEL1L as a novel treatment approach for cancer, focusing on the molecular processes of SEL1L and its involvement in cancer etiology.
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A complex sequence of occurrences, including host genetic vulnerability, Helicobacter pylori infection, and other environmental variables, culminate in gastric cancer (GC). The development of several genetic and epigenetic changes in oncogenes and tumor suppressor genes causes dysregulation of several signaling pathways, which upsets the cell cycle and the equilibrium between cell division and apoptosis, leading to GC. Developments in computational biology and RNA-seq technology enable quick detection and characterization of long non-coding RNAs (lncRNAs). Recent studies have shown that long non-coding RNAs (lncRNAs) have multiple roles in the development of gastric cancer. These lncRNAs interact with molecules of protein, RNA, DNA, and/or combinations. This review article explores several gastric cancer-associated lncRNAs, such as ADAMTS9-AS2, UCA1, XBP-1, and LINC00152. These various lncRNAs could change GC cell apoptosis, migration, and invasion features in the tumor microenvironment. This review provides an overview of the most recent research on lncRNAs and GC cell apoptosis, migration, invasion, and drug resistance, focusing on studies conducted in cancer cells and healthy cells during differentiation.
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Apoptosis , Regulación Neoplásica de la Expresión Génica , MicroARNs , ARN Largo no Codificante , Neoplasias Gástricas , Neoplasias Gástricas/genética , Neoplasias Gástricas/patología , Humanos , ARN Largo no Codificante/genética , MicroARNs/genética , Apoptosis/genética , Microambiente Tumoral/genética , Movimiento Celular/genética , Transducción de Señal/genética , Resistencia a Antineoplásicos/genéticaRESUMEN
Long noncoding RNAs (lncRNAs) are a category of noncoding RNAs characterized by their length, often exceeding 200 nucleotides. There is a growing body of data that indicate the significant involvement of lncRNAs in a wide range of disorders, including cancer. lncRNA H19 was among the initial lncRNAs to be identified and is transcribed from the H19 gene. The H19 lncRNA exhibits significant upregulation in a diverse range of human malignancies, such as breast, colorectal, pancreatic, glioma, and gastric cancer. Moreover, the overexpression of H19 is frequently associated with a worse prognosis among individuals diagnosed with cancer. H19 has been shown to have a role in facilitating several cellular processes, including cell proliferation, invasion, migration, epithelial-mesenchymal transition, metastasis, and apoptosis. This article summarizes the aberrant upregulation of H19 in human malignancies, indicating promising avenues for future investigations on cancer diagnostics and therapeutic interventions.
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Neoplasias , ARN Largo no Codificante , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Humanos , Neoplasias/genética , Neoplasias/patología , Neoplasias/metabolismo , Transición Epitelial-Mesenquimal/genética , Proliferación Celular , Apoptosis , Regulación Neoplásica de la Expresión Génica , Movimiento CelularRESUMEN
Nucleic acid vaccines (NAVs) have the potential to be economical, safe, and efficacious. Furthermore, just the chosen antigen in the pathogen is the target of the immune responses brought on by NAVs. Triple-negative breast cancer (TNBC) treatment shows great promise for nucleic acid-based vaccines, such as DNA (as plasmids) and RNA (as messenger RNA [mRNA]). Moreover, cancer vaccines offer a compelling approach that can elicit targeted and long-lasting immune responses against tumor antigens. Bacterial plasmids that encode antigens and immunostimulatory molecules serve as the foundation for DNA vaccines. In the 1990s, plasmid DNA encoding the influenza A nucleoprotein triggered a protective and targeted cytotoxic T lymphocyte (CTL) response, marking the first instance of DNA vaccine-mediated immunity. Similarly, in vitro transcribed mRNA was first successfully used in animals in 1990. At that point, mice were given an injection of the gene encoding the mRNA sequence, and the researchers saw the production of a protein. We begin this review by summarizing our existing knowledge of NAVs. Next, we addressed NAV delivery, emphasizing the need to increase efficacy in TNBC.
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Neoplasias de la Mama Triple Negativas , Vacunas de ADN , Humanos , Ratones , Animales , Vacunación Basada en Ácidos Nucleicos , Neoplasias de la Mama Triple Negativas/terapia , Neoplasias de la Mama Triple Negativas/patología , Inmunoterapia , ADN , ARN Mensajero/genéticaRESUMEN
Cerebral ischemic damage is prevalent and the second highest cause of death globally across patient populations; it is as a substantial reason of morbidity and mortality. Mesenchymal stromal cells (MSCs) have garnered significant interest as a potential treatment for cerebral ischemic damage, as shown in ischemic stroke, because of their potent intrinsic features, which include self-regeneration, immunomodulation, and multi-potency. Additionally, MSCs are easily obtained, isolated, and cultured. Despite this, there are a number of obstacles that hinder the effectiveness of MSC-based treatment, such as adverse microenvironmental conditions both in vivo and in vitro. To overcome these obstacles, the naïve MSC has undergone a number of modification processes to enhance its innate therapeutic qualities. Genetic modification and preconditioning modification (with medications, growth factors, and other substances) are the two main categories into which these modification techniques can be separated. This field has advanced significantly and is still attracting attention and innovation. We examine these cutting-edge methods for preserving and even improving the natural biological functions and therapeutic potential of MSCs in relation to adhesion, migration, homing to the target site, survival, and delayed premature senescence. We address the use of genetically altered MSC in stroke-induced damage. Future strategies for improving the therapeutic result and addressing the difficulties associated with MSC modification are also discussed.
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Isquemia Encefálica , Precondicionamiento Isquémico , Accidente Cerebrovascular Isquémico , Trasplante de Células Madre Mesenquimatosas , Células Madre Mesenquimatosas , Accidente Cerebrovascular , Humanos , Accidente Cerebrovascular Isquémico/metabolismo , Isquemia Encefálica/terapia , Isquemia Encefálica/metabolismo , Accidente Cerebrovascular/terapia , Accidente Cerebrovascular/metabolismo , Precondicionamiento Isquémico/métodos , Células Madre Mesenquimatosas/metabolismoRESUMEN
About 70% of cases of breast cancer are compromised by Estrogen-positive breast cancer. Through its regulation of several processes, including cell proliferation, cell cycle progression, and apoptosis, Estrogen signaling plays a pivotal role in the genesis and progression of this particular kind of breast cancer. One of the best treatment strategies for treating Estrogen-positive breast cancer is blocking Estrogen signaling. However, patients' treatment failure is mainly caused by the emergence of resistance and metastases, necessitating the development of novel therapeutic targets. Numerous studies have shown long noncoding RNAs (lncRNAs) to play a role in Estrogen-mediated carcinogenesis. These lncRNAs interact with co-regulators and the Estrogen signaling cascade components, primarily due to Estrogen activation. Vimentin and E-cadherin are examples of epithelial-to-mesenchymal transition markers, and they regulate genes involved in cell cycle progression, such as Cyclins, to affect the growth, proliferation, and metastasis of Estrogen-positive breast cancer. Furthermore, a few of these lncRNAs contribute to developing resistance to chemotherapy, making them more desirable targets for enhancing results. Thus, to shed light on the creation of fresh approaches for treating this cancer, this review attempts to compile recently conducted studies on the relationship between lncRNAs and the advancement of Estrogen-positive breast cancer.
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Neoplasias de la Mama , ARN Largo no Codificante , Humanos , Femenino , Neoplasias de la Mama/patología , ARN Largo no Codificante/genética , Estrógenos , Proliferación Celular/genética , Receptores de Estrógenos/metabolismo , Regulación Neoplásica de la Expresión GénicaRESUMEN
Nuclear paraspeckle assembly transcript 1 (NEAT1) is a long noncoding RNA (lncRNA) that is widely expressed in a variety of mammalian cell types. Altered expression levels of the lncRNA NEAT1 have been reported in liver-related disorders including cancer, fatty liver disease, liver fibrosis, viral hepatitis, and hepatic ischemia. lncRNA NEAT1 mostly acts as a competing endogenous RNA (ceRNA) to sponge various miRNAs (miRs) to regulate different functions. In regard to hepatic cancers, the elevated expression of NEAT1 has been reported to have a relation with the proliferation, migration, angiogenesis, apoptosis, as well as epithelial-mesenchymal transition (EMT) of cancer cells. Furthermore, NEAT1 upregulation has contributed to the pathogenesis of other liver diseases such as fibrosis. In this review, we summarize and discuss the molecular mechanisms by which NEAT1 contributes to liver-related disorders including acute liver failure, nonalcoholic fatty liver disease (NAFLD), liver fibrosis, and liver carcinoma, providing novel insights and introducing NEAT1 as a potential therapeutic target in these diseases.
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MicroARNs , Enfermedad del Hígado Graso no Alcohólico , ARN Largo no Codificante , Animales , Humanos , Proliferación Celular/genética , Fibrosis , Cirrosis Hepática/genética , Mamíferos/genética , Mamíferos/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , Enfermedad del Hígado Graso no Alcohólico/genética , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismoRESUMEN
Diabetic foot ulcer (DFU) is associated with long-term hospitalization and amputation. Antibiotic resistance has made the infection eradication more difficult. Hence, seeking alternative therapies such as phage therapy seems necessary. Bacteriophages are viruses targeting specific bacterial species. Klebsiella pneumoniae (K. pneumoniae) is among causative agents of the DFU. In this study, the therapeutic effects of single phage and phage cocktail were investigated against multidrug-resistant (MDR) K. pneumonia isolated from DFU. Bacteriophages were isolated from animal feces and sewage samples, and were enriched and propagated using K. pneumoniae as the host. Thirty K. pneumoniae clinical isolates were collected from hospitalized patients with DFU. The antibiotic susceptibility pattern was determined using agar disk diffusion test. The phages' morphological traits were determined using transmission electron microscopy (TEM). The killing effect of isolated phages was assessed using plaque assay. Four phage types were isolated and recognized including KP1, KP2, KP3, and KP4. The bacterial rapid regrowth was observed following each single phage-host interaction, but not phage cocktail due to the evolution of mutant strains. Phage cocktail demonstrated significantly higher antibacterial activity than each single phage (p < 0.05) without any bacterial regrowth. The employment of phage cocktail was promising for the eradication of MDR-K. pneumoniae isolates. The development of phage therapy in particular, phage cocktail is promising as an efficient approach to eradicate MDR-K. pneumoniae isolated from DFU. The application of a specific phage cocktail can be investigated to try and achieve the eradication of various infections.
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Bacteriófagos , Diabetes Mellitus , Pie Diabético , Terapia de Fagos , Animales , Bacteriófagos/genética , Klebsiella pneumoniae , Pie Diabético/terapia , Antibacterianos/farmacología , Antibacterianos/uso terapéuticoRESUMEN
Cholesterol is an essential lipid that serves several important functions, including maintaining the homeostasis of cells, acting as a precursor to bile acid and steroid hormones and preserving the stability of membrane lipid rafts. 25-hydroxycholesterol (25-HC) is a cholesterol derivative that may be formed from cholesterol. 25-HC is a crucial component in various biological activities, including cholesterol metabolism. In recent years, growing evidence has shown that 25-HC performs a critical function in the etiology of cancer, infectious diseases and autoimmune disorders. This review will summarize the latest findings regarding 25-HC, including its biogenesis, immunomodulatory properties and role in innate/adaptive immunity, inflammation and the development of various types of cancer.
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Hidroxicolesteroles , Neoplasias , Humanos , Hidroxicolesteroles/metabolismo , Colesterol/metabolismo , Inmunidad Innata , Neoplasias/etiologíaRESUMEN
Genital tract infections can cause a variety of harmful health outcomes, including endometritis, bacterial vaginosis, and pelvic inflammatory disease, in addition to infertility. Anaerobic bacteria, such as Gardnerella vaginalis, Megasphaera spp., and Atopobium vaginae, are more commonly identified in cases of bacterial vaginosis than lactobacilli. It is unknown how the microorganisms that cause pelvic inflammatory diseases and endometritis enter the uterus. Both prospective and retrospective research have connected pelvic inflammatory disorders, chronic endometritis, and bacterial vaginosis to infertility. Similar to bacterial vaginosis, endometritis-related infertility is probably caused by a variety of factors, such as inflammation, immune system recognition of sperm antigens, bacterial toxins, and a higher risk of STDs. Preconception care for symptomatic women may include diagnosing and treating pelvic inflammatory disease, chronic endometritis, and bacterial vaginosis before conception to optimize the results of both natural and assisted reproduction.
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Endometritis , Vaginosis Bacteriana , Humanos , Femenino , Embarazo , Vaginosis Bacteriana/inmunología , Vaginosis Bacteriana/microbiología , Vaginosis Bacteriana/diagnóstico , Endometritis/inmunología , Endometritis/microbiología , Endometritis/diagnóstico , Infertilidad Femenina/inmunología , Infertilidad Femenina/microbiología , Enfermedad Inflamatoria Pélvica/inmunología , Enfermedad Inflamatoria Pélvica/microbiología , Enfermedad Inflamatoria Pélvica/diagnóstico , Sistema Inmunológico/inmunología , Infecciones Bacterianas/inmunología , Infecciones Bacterianas/microbiología , Infecciones Bacterianas/diagnóstico , Complicaciones Infecciosas del Embarazo/inmunología , Complicaciones Infecciosas del Embarazo/microbiología , Complicaciones Infecciosas del Embarazo/diagnósticoRESUMEN
Metastatic cancer, which accounts for the majority of cancer fatalities, is a difficult illness to treat. Currently used cancer treatments include radiation therapy, chemotherapy, surgery, and targeted treatment (immune, gene, and hormonal). The disadvantages of these treatments include a high risk of tumor recurrence and surgical complications that may result in permanent deformities. On the other hand, most chemotherapy drugs are small molecules, which usually have unfavorable side effects, low absorption, poor selectivity, and multi-drug resistance. Anticancer drugs can be delivered precisely to the cancer spot by encapsulating them to reduce side effects. Stimuli-responsive nanocarriers can be used for drug release at cancer sites and provide target-specific delivery. As previously stated, metastasis is the primary cause of cancer-related mortality. We have evaluated the usage of nano-medications in the treatment of some metastatic tumors.
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Antineoplásicos , Neoplasias , Humanos , Resistencia a Antineoplásicos , Neoplasias/tratamiento farmacológico , Antineoplásicos/farmacología , Resistencia a Múltiples MedicamentosRESUMEN
The expression of the nuclear paraspeckle assembly transcript 1 (NEAT1), as a well-known long non-coding RNA (lncRNA), is often upregulated in varied types of cancers and associated with poor survival outcomes in patients suffering from tumors. NEAT1 promotes the tumors growth by influencing the various genes' expression profile that regulate various aspects of tumor cell behavior, in particular tumor growth, metastasis and drug resistance. This suggests that NEAT1 are capable of serving as a new diagnostic biomarker and target for therapeutic intervention. Through interrelation with enhancer of zeste homolog 2 (EZH2), NEAT1 acts as a scaffold RNA molecule, and thus regulating the expression EZH2-associated genes. Additionally, by perform as miRNA sponge, it constrains suppressing the interactions between miRNAs-mediated degradation of target mRNAs. In light of this, NEAT1 inhibition by small interfering RNA (siRNA) hampers tumorgenesis. We summarize recent findings about the expression, biological functions, and regulatory process of NEAT1 in human tumors. It specifically emphasizes the clinical significance of NEAT1 as a novel diagnostic biomarker and a promising therapeutic mark for many types of cancers.
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Proteína Potenciadora del Homólogo Zeste 2 , Neoplasias , ARN Largo no Codificante , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Humanos , Neoplasias/genética , Neoplasias/patología , Neoplasias/metabolismo , Proteína Potenciadora del Homólogo Zeste 2/metabolismo , Proteína Potenciadora del Homólogo Zeste 2/genética , Proteína Potenciadora del Homólogo Zeste 2/antagonistas & inhibidores , Metástasis de la Neoplasia , Regulación Neoplásica de la Expresión Génica , MicroARNs/genética , MicroARNs/metabolismo , Biomarcadores de Tumor/genética , Biomarcadores de Tumor/metabolismo , ARN Interferente Pequeño/metabolismo , Carcinogénesis/genéticaRESUMEN
The cancer cells that are not normal can grow into tumors, invade surrounding tissues, and travel to other parts of the body via the lymphatic or circulatory systems. Interleukins, a vital class of signaling proteins, facilitate cell-to-cell contact within the immune system. A type of non-coding RNA known as lncRNAs mediates its actions by regulating miRNA-mRNA roles (Interleukins). Because of their dual function in controlling the growth of tumors and altering the immune system's response to cancer cells, interleukins have been extensively studied concerning cancer. Understanding the complex relationships between interleukins, the immune system, the tumor microenvironment, and the components of interleukin signaling pathways that impact the miRNA-mRNA axis, including lncRNAs, has advanced significantly in cancer research. Due to the significant and all-encompassing influence of interleukins on the immune system and the development and advancement of cancers, lncRNAs play a crucial role in cancer research by modulating interleukins. Their diverse effects on immune system regulation, tumor growth encouragement, and tumor inhibition make them appealing candidates for potential cancer treatments and diagnostics. A deeper understanding of the relationship between the biology of interleukin and lncRNAs will likely result in more effective immunotherapy strategies and individualized cancer treatments.
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Interleucinas , Neoplasias , ARN Largo no Codificante , Microambiente Tumoral , Animales , Humanos , Regulación Neoplásica de la Expresión Génica , Interleucinas/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , Neoplasias/inmunología , Neoplasias/patología , Neoplasias/metabolismo , Neoplasias/genética , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Transducción de Señal/fisiología , Microambiente Tumoral/inmunologíaRESUMEN
Electrochemical techniques are commonly used to analyze and screen various environmental pathogens. When used in conjunction with other optical recognition methods, it can extend the sensing range, lower the detection limit, and offer mutual validation. Nowadays, electrochemical-optical dual-mode biosensors have ensured the accuracy of test results by integrating two signals into one, indicating their potential use in primary food safety quantitative assays and screening tests. Particularly, visible optical signals from electrochemical/colorimetric dual-mode biosensors could meet the demand for real-time screening of microbial pathogens. While electrochemical-optical dual-mode probes have been receiving increasing attention, there is limited emphasis on the design approaches for sensors intended for microbial pathogens. Here, we review the recent progress in the merging of optical and electrochemical techniques, including fluorescence, colorimetry, surface plasmon resonance (SPR), and surface enhanced Raman spectroscopy (SERS). This study particularly emphasizes the reporting of various sensing performances, including sensing principles, types, cutting-edge design approaches, and applications. Finally, some concerns and upcoming advancements in dual-mode probes are briefly outlined.
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Técnicas Biosensibles , Técnicas Biosensibles/métodos , Resonancia por Plasmón de Superficie/métodos , Técnicas Electroquímicas/métodos , Inocuidad de los Alimentos , ColorimetríaRESUMEN
Chimeric Antigen Receptor (CAR) based therapies are becoming increasingly important in treating patients. CAR-T cells have been shown to be highly effective in the treatment of hematological malignancies. However, harmful therapeutic barriers have been identified, such as the potential for graft-versus-host disease (GVHD), neurotoxicity, and cytokine release syndrome (CRS). As a result, CAR NK-cell therapy is expected to be a new therapeutic option. NK cells act as cytotoxic lymphocytes, supporting the innate immune response against autoimmune diseases and cancer cells by precisely detecting and eliminating malignant cells. Genetic modification of these cells provides a dual approach to the treatment of AD and cancer. It can be used through both CAR-independent and CAR-dependent mechanisms. The use of CAR-based cell therapies has been successful in treating cancer patients, leading to further investigation of this innovative treatment for alternative diseases, including AD. The complementary roles of CAR T and CAR NK cells have stimulated exploration in this area. Our study examines the latest research on the therapeutic effectiveness of these cells in treating both cancer and ADs.
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Enfermedades Autoinmunes , Inmunoterapia Adoptiva , Células Asesinas Naturales , Neoplasias , Receptores Quiméricos de Antígenos , Humanos , Células Asesinas Naturales/inmunología , Células Asesinas Naturales/trasplante , Receptores Quiméricos de Antígenos/inmunología , Neoplasias/terapia , Neoplasias/inmunología , Enfermedades Autoinmunes/terapia , Enfermedades Autoinmunes/inmunología , Inmunoterapia Adoptiva/métodos , AnimalesRESUMEN
Pre-messenger RNA molecules are back-spliced to create circular RNAs, which are non-coding RNA molecules. After a thorough investigation, it was discovered that these circRNAs have critical biological roles. CircRNAs have a variety of biological functions, including their ability to operate as microRNA sponges, interact with proteins to alter their stabilities and activities, and provide templates for the translation of proteins. Evidence supports a link between the emergence of numerous diseases, including various cancer types, and dysregulated circRNA expression. It is commonly known that a significant contributing element to cancer development is the disruption of numerous molecular pathways essential for preserving cellular and tissue homeostasis. The dysregulation of multiple biological processes is one of the hallmarks of cancer, and the molecular pathways linked to these processes are thought to be promising targets for therapeutic intervention. The biological and carcinogenic effects of circRNAs in the context of cancer are thoroughly reviewed in this article. Specifically, we highlight circRNAs' involvement in signal transduction pathways and their possible use as novel biomarkers for the early identification and prognosis of human cancer.
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MicroARNs , Neoplasias , Humanos , ARN Circular/genética , Neoplasias/genética , Neoplasias/patología , ARN Mensajero , Transducción de Señal/genéticaRESUMEN
At first, an organometallic catalyst namely, Pd-DPyE@MCM-41@MNP was prepared through magnetic (Fe3O4) nanoparticles-doped into channels of mesoporous silica MCM-41 and then, anchoring a novel complex composed of di(4-pyridyl)ethylene and palladium on the inner surface of the support. This immobilized catalyst was successfully identified via VSM, ICP-OES, TEM, FTIR, TGA, SEM, BET, XRD, EDX and elemental mapping analyses. After that, it was used as a versatile, heterogeneous, and magnetically reproducible catalyst in the generation of N,N'-alkylidene bisamides (1a-13a, 8-20 min, 90-98%, 50 °C, solvent-free) and Suzuki-Miyaura coupling (SMC) reaction derivatives (1b-26b, 10-140 min, 86-98%, 60 °C, PEG-400). The VSM plot of Pd-DPyE@MCM-41@MNP displays that this nanocatalyst can be easily recycled by applying an external magnetic field. In both synthetic paths, this nanocatalyst was reused at least seven times without palladium leaching and significantly reducing its catalytic performance. Also, stability and heterogeneous nature of catalyst were approved via ICP-OES technique and hot filtration test.
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Oral Squamous Cell Carcinoma (OSCC) is the most common type of head and neck cancer worldwide. Emerging research suggests a strong association between OSCC and the oral microbiota, a diverse community of bacteria, fungi, viruses, and archaea. Pathogenic bacteria, in particular Porphyromonas gingivalis and Fusobacterium nucleatum, have been closely linked to OSCC. Moreover, certain oral fungi, such as Candida albicans, and viruses, like the human papillomavirus, have also been implicated in OSCC. Despite these findings, the precise mechanisms through which the oral microbiota influences OSCC development remain unclear and necessitate further research. This paper provides a comprehensive overview of the oral microbiota and its relationship with OSCC and discusses potential carcinogenic pathways that the oral microbiota may activate or modulate are also discussed.
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Cancer drug resistance remains a formidable challenge in modern oncology, necessitating innovative therapeutic strategies. The convergence of intricate regulatory networks involving long non-coding RNAs, microRNAs, and pivotal signaling pathways has emerged as a crucial determinant of drug resistance. This review underscores the multifaceted roles of lncRNAs and miRNAs in orchestrating gene expression and cellular processes, mainly focusing on their interactions with specific signaling pathways. Dysregulation of these networks leads to the acquisition of drug resistance, dampening the efficacy of conventional treatments. The review highlights the potential therapeutic avenues unlocked by targeting these non-coding RNAs. Developing specific inhibitors or mimics for lncRNAs and miRNAs, alone or in combination with conventional chemotherapy, emerges as a promising strategy. In addition, epigenetic modulators, immunotherapies, and personalized medicine present exciting prospects in tackling drug resistance. While substantial progress has been made, challenges, including target validation and safety assessment, remain. The review emphasizes the need for continued research to overcome these hurdles and underscores the transformative potential of lncRNA-miRNA interplay in revolutionizing cancer therapy.
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MicroARNs , Neoplasias , ARN Largo no Codificante , Humanos , MicroARNs/genética , ARN Largo no Codificante/genética , Resistencia a Antineoplásicos/genética , Inmunoterapia , Transducción de Señal/genética , Neoplasias/tratamiento farmacológico , Neoplasias/genéticaRESUMEN
Having been involved in complex cellular regulatory networks and cell-to-cell communications, non-coding RNAs (lncRNAs) have become functional carriers that transmit information between cells and tissues, modulate tumor microenvironments, encourage angiogenesis and invasion, and make tumor cells more resistant to drugs. Immune cells' exosomal lncRNAs may be introduced into tumor cells to influence the tumor's course and the treatment's effectiveness. Research has focused on determining if non-coding RNAs affect many target genes to mediate regulating recipient cells. The tumor microenvironment's immune and cancer cells are influenced by lncRNAs, which may impact a treatment's efficacy. The lncRNA-mediated interaction between cancer cells and immune cells invading the tumor microenvironment has been the subject of numerous recent studies. On the other hand, tumor-derived lncRNAs' control over the immune system has not gotten much attention and is still a relatively new area of study. Tumor-derived lncRNAs are recognized to contribute to tumor immunity, while the exact mechanism is unclear.