CASC19: An Oncogenic Long Non-coding RNA in Different Cancers.

A 324 bp lncRNA called CASC19 is found on chromosome 8q24.21. Recent research works have revealed that CASC19 is involved in the prognosis of tumors and related to the regulation of the radiation tolerance mechanisms during tumor radiotherapy (RT). This review sheds light on the changes and roles that CASC19 plays in many tumors and diseases, such as nasopharyngeal carcinoma (NPC), cervical cancer, colorectal cancer (CRC), non-small cell lung cancer (NSCLC), clear cell renal cell carcinoma (ccRCC), gastric cancer (GC), pancreatic cancer (PC), hepatocellular carcinoma (HCC), glioma, and osteoarthritis (OA). CASC19 provides a new strategy for targeted therapy, and the regulatory networks of CASC19 expression levels play a key role in the occurrence and development of tumors and diseases. In addition, the expression level of CASC19 has predictive roles in the prognosis of some tumors and diseases, which has major implications for clinical diagnoses and treatments. CASC19 is also unique in that it is a key gene affecting the efficacy of RT in many tumors, and its expression level plays a decisive role in improving the success rate of treatments. Further research is required to determine the precise process by which CASC19 causes changes in diseased cells in some tumors and diseases.

Application of Nanomedicine in Tumor Targeting Inflammatory Pathway.

Given the threat of ever-growing cancer morbidity, it is a cutting-edge frontier for multiple disciplines to apply nanotechnology in cancer therapy. Nanomedicine is now perpetually influencing the diagnosis and treatment of cancer. Meanwhile, tumorigenesis and cancer progression are intimately associated with inflammation. Inflammation can implicate in various tumor progression via the same or different pathways. Therefore, current nanomedicines exhibit tumor-suppressing function through inflammatory pathways. At present, the comprehensive understanding and research on the mechanism of various nanoparticles in cancer treatment are still in progress. In this review, we summarized the applications of nanomedicine in tumor-targeting inflammatory pathways, suggesting that nanoparticles could be a budding star for cancer therapy.

SNHG11: A New Budding Star in Tumors and Inflammatory Diseases.

BACKGROUND: Long non-coding RNAs (lncRNAs) are transcripts that are over 200 nucleotides in length and lack protein-coding potential. Despite their name, lncRNAs have important regulatory roles in transcription, translation, and protein function by interacting with DNA, RNA, and protein molecules. Small nucleolar RNAs (snoRNAs), found in various tumors, are encoded by lncRNAs and have gained attention in recent research. The lncRNAs, encoding snoRNAs are known as small nucleolar RNA host genes (SNHGs), a newly identified class of lncRNAs. SNHG11, a specific SNHG, is a critical regulatory factor involved in various biological processes. Accumulating evidence suggests that SNHG11 can impact tumor development and inflammatory diseases by modulating downstream gene expression through chromatin modification, transcription, or post-transcriptional mechanisms. The expression levels of SNHG11 vary significantly in different normal tissues, tumors, and stages of tumor development. Currently, treatment options for advanced cancers are mainly palliative and lack curative potential. OBJECTIVES: This review aims to explore the modifications and functions of lncRNA SNHG11 in various tumors and inflammatory diseases. Through a comprehensive analysis of relevant literature on SNHG11 in PubMed, the review aims to provide a comprehensive description of the roles of SNHG11 in known tumors and inflammatory diseases and elucidate the specific mechanism's underlying functions. The changes in SNHG11 expression in tumors and inflammatory diseases can serve as early biomarkers, therapeutic targets, and prognostic indicators. Improving the clinical detection, staging, treatment, and prognosis of tumors is of great value. Additionally, the structural modifications of SNHG11 can potentially enhance its function as a drug carrier to maximize the therapeutic potential of drugs. Furthermore, understanding the specific mechanisms of SNHG11 in tumors and inflammatory diseases may provide new ways for targeted therapy. MATERIALS AND METHODS: Relevant studies were retrieved and collected from the PubMed system. SNHG11 was identified as the research object, and research literature on SNHG11 in the past ten years was analyzed to determine its strong association with the onset and progression of various diseases. The precise mechanisms of SNHG11's mode of action were reviewed, and references were further determined based on their impact factors for comprehensive analysis. RESULTS: Through review and analysis, it was found that SNHG11 is involved in a wide range of tumors and inflammatory diseases through its high expression, including lung cancer, colorectal cancer, prostate cancer, hepatocellular carcinoma, triple-negative breast cancer, gastric cancer, glioma, ovarian cancer, pancreatic cancer, acute pancreatitis, and ischemic stroke, but with lower expression in virus myocarditis. SNHG11 is abnormally expressed in cells of these tumors and inflammatory diseases mainly contributes to disease proliferation, metastasis, ceRNA activity, miRNA sponging, drug resistance, and tumor prognosis. However, the specific mechanisms of SNHG11 in tumors and inflammatory diseases require further detailed exploration. Understanding the known regulatory mechanisms can expand the scope of clinical applications and promote early clinical detection, monitoring, and treatment. CONCLUSION: LncRNA SNHG11 can serve as an early diagnostic biomarker, therapeutic target, and prognostic indicator in various diseases, particularly tumors. SNHG11 plays a crucial role in the occurrence and development of tumors and inflammatory diseases through various mechanisms, which has significant implications for clinical diagnosis and treatment.

The regulatory role of LncRNA HCG18 in various cancers.

As a member of long non-coding RNAs (lncRNAs), LncRNA HLA complex group 18 (HCG18) has recently become the focus of cancer research. As outlined in this review, LncRNA HCG18 has been reported to be dysregulated in various cancers development and appears to be activated in a variety of tumors, including clear cell renal cell carcinoma (ccRCC), colorectal cancer (CRC), gastric cancer (GC), hepatocellular carcinoma (HCC), laryngeal and hypopharyngeal squamous cell carcinoma (LHSCC), lung adenocarcinoma (LUAD), nasopharyngeal cancer (NPC), osteosarcoma (OS), and prostate cancer (PCa). Furthermore, the expression of lncRNA HCG18 decreased in bladder cancer (BC) and papillary thyroid cancer (PTC). Overall, the presence of these differential expressions suggests the clinical value of HCG18 in cancer therapy. Additionally, lncRNA HCG18 influences various biological processes of cancer cells. This review summarizes the molecular mechanisms of HCG18 in cancer development, highlights reported the abnormal expression of HCG18 found in various cancer types, and aims to discuss the potential of HCG18 as a target for cancer therapy.

The Functions of EphA1 Receptor Tyrosine Kinase in Several Tumors.

BACKGROUND: Eph receptors tyrosine kinase (RTK) were identified in 1987 from hepatocellular carcinoma cell lines and were the largest known subfamily of RTK. Eph receptors can be divided into two categories, EphA and EphB, based on their structure and receptor-ligand specificity. EphA can be divided into 10 species (EphA 1-10) and EphB into 6 species (EphB1-6). Similarly, the ligands of Eph receptors are Ephrins. Ephrins also can be divided into Ephrin A and Ephrin B, of which there are five species(Ephrin-A1-5) and three species(Ephrin-B1-3). Among the Eph receptors, EphA1 has been the least studied so far. As far as we know, Eph receptors are involved in multiple pathologies, including cancer progression, tumor angiogenesis, intestinal environmental stability, the lymph node system, neurological disease, and inhibition of nerve regeneration after injury. There is a link between EphA1, integrin and ECM- related signal pathways. Ephrin-A1 is a ligand of the EphA1 receptor. EphA1 and ephrin-A1 functions are related to tumor angiogenesis. EphA1 and ephrin-A1 also play roles in gynecological diseases. Ephrin-A1 and EphA1 receptors regulate the follicular formation, ovulation, embryo transport, implantation and placental formation, which are of great significance for the occurrence of gynecological tumor diseases. EphA1 has been identified as an oncoprotein in various tumors and has been associated with the prognosis of various tumors in recent years. EphA1 is considered a driver gene in tumor genomics. There are significant differences in EphA1 expression levels in different types of normal tissues and tumors and even in different stages of tumor development, suggesting its functional diversity. Changes at the gene level in cell biology are often used as biological indicators of cancer, known as biomarkers, which can be used to provide diagnostic or prognostic information and are valuable for improving the detection, monitoring and treatment of tumors. However, few prognostic markers can selectively predict clinically significant tumors with poor prognosis. These malignancies are more likely to progress and lead to death, requiring more aggressive treatment. Currently available treatments for advanced cancer are often ineffective, and treatment options are mainly palliative. Therefore, early identification and treatment of those at risk of developing malignant tumors are crucial. Although pieces of evidence have shown the role of EphA1 in tumorigenesis and development, its specific mechanism is still unknown to a great extent. OBJECTIVE: This review reveals the changes and roles of EphA1 in many tumors and cancers. The change of EphA1 expression can be used as a biological marker of cancer, which is valuable for improving tumor detection, monitoring and treatment and can be applied to imaging. Studies have shown that structural modification of EphA1 could make it an effective new drug. EphA1 is unique in that it can be considered a prognostic marker in many tumors and is of important meaning for clinical diagnosis and operative treatment. At the same time, the study of the specific mechanism of EphA1 in tumors can provide a new way for targeted therapy. METHODS: Relevant studies were retrieved and collected through the PubMed system. After determining EphA1 as the research object, by analyzing research articles on EphA1 in the PubMed system in recent 10 years, we found that EphA1 was closely connected with the occurrence and development of tumors and further determined the references according to the influencing factors for review and analysis. RESULTS: EphA1 has been identified as a cancer protein in various tumors, such as hepatocellular carcinoma, nasopharyngeal carcinoma, ovarian cancer, gastric cancer, colorectal cancer, clear cell renal cell carcinoma, esophageal squamous cell carcinoma, breast cancer, prostate cancer and uveal melanoma. EphA1 is abnormally expressed in these tumor cells, which mainly plays a role in cancer progression, tumor angiogenesis, intestinal environmental stability, the lymph node system, nervous system diseases and gynecological diseases. In a narrow sense, EphA1 is especially effective in breast cancer in terms of gynecological diseases. However, the specific mechanism of EphA1 leading to the change of cancer cells in some tumors is not clear, which needs further research and exploration. CONCLUSION: RTK EphA1 can be used as a biomarker for tumor diagnosis (especially a prognostic marker), an indispensable therapeutic target for new anti-tumor therapies, and a novel anti-tumor drug.

WDFY3-AS2: A Potential Prognostic Factor and Therapeutic Target Related to Cancer.

BACKGROUND: Abundant studies have shown that non-coding RNA is connected with tumor cell growth, migration and invasion. As a newly discovered non-coding RNA, WDFY3-AS2 has gradually emerged in the molecular mechanism of various tumors and has a potential prospect as a biological indicator of tumor prognosis. This review describes the pathophysiological mechanism and prognostic value of WDFY3-AS2 in different cancers. OBJECTIVE: This review reveals the changes and roles of WDFY3-AS2 in many tumors and cancers. The change of WDFY3-AS2 can be used as a cancer biomarker and plays an important role in improving tumor growth, migration and invasion. WDFY3-AS2 is unique because it can be considered a prognostic marker for many tumors and is of great significance for clinical diagnosis and treatment. WDFY3-AS2 shows the potential prognostic value and the prospect of therapeutic targets in various tumors. METHODS: PubMed reviewed the related literature to analyze and summarize the regulatory molecular mechanism of WDFY3-AS2 in various tumors and its value as a prognostic indicator. RESULTS: The abnormal expression of LncRNA WDFY3-AS2 in many cancers was connected with the poor prognosis of cancer patients, including diffuse glioma, hepatocellular carcinoma, ovarian cancer, esophageal cancer, triple-negative breast cancer, Clear Cell Renal Carcinoma, Esophageal squamous cell carcinoma, Lung adenocarcinoma, which participated in the recovery of orthodontic teeth. WDFY3-AS2 has revealed the cellular process of cancer cell growth, migration, and invasion. CONCLUSION: The molecular mechanism of LncRNA WDFY3-AS2 regulating tumor specifically proves that WDFY3-AS2 has a good prospect in the biological index of prognosis or clinical treatment target of cancer patients.

The Dual Functions of Non-Coding RNA CRNDE in Different Tumors.

Long non-coding RNA has attracted the interest of researchers as a relevant factor that can influence human cancers. As an oncogene and suppressor gene, it has numerous pathways and is closely related to the pathophysiology of human diseases. Meanwhile, it may become a novel treatment option and target for tumor treatment. CRNDE is the gene symbol for Colorectal Neoplasia Differentially Expressed (non-protein-coding) since it was found to be considerably higher in colorectal cancer when it was first discovered. It's transcribed from human chromosome 16. Many studies have shown that it is intimately linked to the etiology of many tumors and malignancies. According to the paper, the biological function and pathophysiological mechanism of CRNDE in tumors have been studied extensively in recent years. PubMed served as an essential platform for conducting literature searches and related analyses. CRNDE, a long non-coding RNA closely related to tumors, was highly expressed in many tumor cells. There were various underlying mechanisms affecting the progression of CRNDE-regulated tumorigenesis, including hepatocellular carcinoma, gastric cancer, prostate carcinoma, oral squamous cell carcinoma, breast cancer, thyroid cancer, myeloma, leukemia, melanoma, colorectal cancer, glioblastoma, osteosarcoma, cervical cancer, intrahepatic cholangiocarcinoma, nonsmall cell lung cancer, hepatoblastoma cell tumor, abdominal aortic aneurysm, nasopharyngeal carcinoma, bladder cancer, Wilms tumor, medulloblastoma, pancreatic cancer, gallbladder cancer, ovarian cancer, and renal cell carcinoma. CRNDE is involved in the processes of proliferation, migration, invasion, and inhibition of apoptosis of various cancer cells.

ITGA9: Potential Biomarkers and Therapeutic Targets in Different Tumors.

Integrins are a class of cell surface adhesion molecules composed of α subunit (ITGA) and ß subunit (ITGB). They belong to heterodimer transmembrane glycoproteins. Their main function in organisms is as the receptor of cell adhesion molecules (CAMs) and extracellular matrix (ECM). According to the current research integration analysis, integrin α9 (ITGA9) is one of the integrin subunits, and there are few studies on ITGA9 among integrins. ITGA9 can improve cell migration and regulate various cellular biological functions, such as tumor cell proliferation, adhesion, invasion, and angiogenesis. However, its abnormal expression mechanism in cancer and its specific role in tumor growth and metastasis are still unknown to a great extent. This review reveals the role of ITGA9 in the complex pathogenesis of many tumors and cancers, providing a new direction for the treatment of tumors and cancers. Relevant studies were retrieved and collected through the PubMed system. After determining ITGA9 as the research object, we found a close relationship between ITGA9 and tumorigenesis by analyzing the research articles on ITGA9 in the PubMed system in the last 15 years and further determined the references mainly based on the influencing factors of the articles. Thus, the role of ITGA9 in tumor and cancer genesis, proliferation, and metastasis was reviewed and analyzed. ITGA9 is an integrin subunit, which has been proved to be abnormally expressed in many tumors. After sorting and analyzing the research data, it was found that the abnormal expression of ITGA9 in a variety of tumors, including glioblastoma, rhabdomyosarcoma, melanoma, hepatocellular carcinoma, nasopharyngeal carcinoma, multiple myeloma, non-small cell lung cancer, and prostate cancer, was closely related to the proliferation, metastasis, adhesion, and angiogenesis of tumor cells. These results suggest that ITGA9 plays an important role in the occurrence and development of tumors. The integrin subunit ITGA9 may serve as a biomarker for the diagnosis of tumors and a potential therapeutic target for anti-tumor therapies.

MEG8: An Indispensable Long Non-coding RNA in Multiple Cancers.

BACKGROUND: As a member of long non-coding RNAs (lncRNAs), maternally expressed gene 8 (MEG8) has been found involving in the progression of a variety of cancers and playing a regulatory role. Therefore, MEG8 may turn into a new therapeutic target for cancer in the future. The purpose of this review is to illustrate the molecular mechanism and physiological function of MEG8 in various cancers. METHODS: We retrieved and analyzed related articles about MEG8, lncRNAs, and cancers, and then summarize the pathophysiological mechanisms of MEG8 in cancer development. RESULTS: LncRNA MEG8 participates in various cancers progression, thus influencing the proliferation, migration, and invasion of cancers. However, the expression of MEG8 is abnormally upregulated in non-small cell lung cancer (NSCLC), pancreatic cancer (PC), liver cancer (HCC), pituitary adenoma (PA) and hemangioma (HA), and inhibited in colorectal cancer (CRC), ovarian cancer (OC) and giant cell tumor (GCT), suggesting its clinical value in cancer therapy. CONCLUSION: LncRNA MEG8 is expected to be a new therapeutic target or biomarker for a wide range of cancers in the future.

LncRNA SBF2-AS1: A Budding Star in Various Cancers.

Long non-coding RNA (lncRNA) is a new kind of RNA with a length of over 200 nucleotides. Current frontiers revealed that lncRNAs implicate in various tumor progression, including tumorigenesis, proliferation, migration, invasion, metastasis, and angiogenesis. Recently discovered long non-coding RNA SETbinding factor 2 antisense RNA 1 (lncRNA SBF2-AS1), an oncogenic antisense RNA to SBF2, locates at 11p15.1 locus and is 2708 nt long. Accumulating evidence has demonstrated that lncRNA SBF2-AS1 participates in the progression of the various tumor, including pathogenesis, diagnosis, treatment, and prognosis of acute myeloid leukemia (AML), breast cancer (BC), cervical cancer (CC), clear cell renal cell carcinoma (ccRCC), colorectal cancer (CRC), diffuse large B-cell lymphoma (DLBCL), esophageal squamous cell carcinoma (ESCC), gastric cancer (GC), glioma, glioblastoma (GBM), hepatocellular carcinoma (HCC), lung cancer (LC), lung adenocarcinoma (LUAD), non-small cell lung cancer (NSCLC), osteosarcoma (OS), pancreatic cancer (PC), papillary thyroid cancer (PTC), small cell lung cancer (SCLC). Therefore, we summarized the underlying mechanisms of lncRNA SBF2-AS1 in various cancers to utilize its therapeutic function in target-selective treatment modalities.

FER1L4: A Long Non-coding RNA with Multiple Roles in the Occurrence and Development of Tumors.

BACKGROUND: FER-1 family member 4 (FER1L4), a 6.7 kb lncRNA located at 20q11.22, plays an important biological function in a variety of tumor diseases. The purpose of this review is to clarify the pathophysiological mechanism and potential biological function of FER1L4 in different tumors. METHODS: By searching the relevant literature in PubMed, the specific pathophysiological mechanism of FER1L4 in different tumors was summarized. RESULTS: LncRNA FER1L4 is one of the key factors in tumorigenesis and is abnormally down-regulated in many tumors, including osteosarcoma, lung cancer, laryngeal squamous cell carcinoma, laryngeal cancer, colorectal cancer, ovarian cancer, prostate cancer, esophageal cancer, gastric cancer, endometrial cancer, osteoarthritis, rheumatoid arthritis, and so on. However, FER1L4 is downregulated in breast cancer, glioma, oral squamous cell carcinoma, renal clear cell carcinoma, and periodontitis, and plays a protective role in orthodontic teeth. In addition, as a tumor suppressor gene or oncogene, FER1L4 affects tumor proliferation, invasion, migration, and apoptosis. CONCLUSION: LncRNA FER1L4 has a good application prospect in the treatment and diagnosis of various tumors.

The Regulatory Role of Both MBNL1 and MBNL1-AS1 in Several Common Cancers.

BACKGROUND: Muscle blind-like-proteins (MBNL) are a class of tissue-specific RNA metabolism regulators that control pre-messenger RNA-splicing. Inactivation of MBNL can lead to myotonic dystrophy in adults. MBNL is mainly expressed in skeletal muscle, neuron tissue, thymus, liver, and kidney and plays an important role in the ultimate differentiation of muscle cells and neurons. MBNL1 is a member of the MBNL protein family. The inactivation of MBNL1 protein is particularly important in the development of myotonic dystrophy and can lead to cataract formation, abnormal muscle relaxation, cardiac and neurological dysfunction, etc. The induction of MBNL1 in tumors is known to significantly inhibit tumor progression and thus significantly prolong survival. MBNL1 antisense protein MBNL1-AS1 also plays an important role in tumor migration and development. OBJECTIVE: This review reveals the role of MBNL1 and MBNL1-AS1 in the complex pathogenesis of many tumors, which provide a new target for the treatment of tumors. METHODS: Correlated research are systematically retrieved via PubMed. In this review, the role of MBNL1 and MBNL1- AS1 were analyzed. RESULTS: MBNL1 is down-regulated in breast cancer, leukemia, stomach cancer, esophageal cancer, glioma, and Huntington's disease. The function of inhibiting tumor cell metastasis decreased. It is up-regulated in cervical cancer and colorectal cancer, which can promote the development of tumor cells. Antisense protein MBNL1- AS1 can inhibit tumor cell proliferation and metastasis in colorectal cancer, non-small cell lung cancer, and gastric cancer. CONCLUSION: MBNL1 is an important regulator of tumor metastasis and growth, which exhibits a promising therapeutic target and can be further explored.