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Cancer is one of the main reasons for death, and it threatens human life and health. Both the environment and genes can lead to cancers. It dates back more than a million years; more importantly, tumor cells can not be detected until they grow to a large number. Currently, cancers are treated with surgical excision or non-surgical procedures. By studying the interaction between ncRNAs and PKM2, we aim to provide new targets for diagnosis, treatment, and prognosis for cancers. Read relevant articles and made a summary and classification. Non-coding RNAs (ncRNAs) are RNAs that do not code for proteins. They perform a function in transcription and translation and can be used as targets for cancer therapy. Pyruvate kinase M2 (PKM2) is a form of PKM, and it catalyzes the glycolysis of the final cellular processes to promote tumorigenesis. Not only that, but it also plays non-metabolic functions, including the expression of the gene, cell proliferation, cell migration, and tumor angiogenesis in cancer cells. The existing studies have found that microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) can promote or inhibit the aerobic glycolysis of cancer cells by affecting PKM2, which increases or decrease the risk of cancers and affect the progression of cancers. This review focuses on the mechanism of ncRNAs regulating PKM2 in cancers and summarizes the roles of some ncRNAs., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Non-coding RNAs are mainly divided into two categories, one is small non-coding RNA represented by miRNA, and the other is long non-coding RNA longer than 200 bp. Further studies on non-coding RNAs have revealed that long non-coding RNAs not only have carcinogenic effects, but also have potential links with miRNAs. Antisense non-coding RNA in the INK4 locus (ANRIL/CDKN2B-AS1), one of the five subtypes of long non-coding RNA, has been proved to play a role of oncogene in many cancers, such as gastric cancer, cervical cancer, prostate cancer and non-small cell lung cancer. Knockdown ANRIL can significantly inhibit the proliferation and migration of cancer cells, while also negatively regulating the expression of related miRNAs. This suggests that ANRIL may serve as a potential target for the development of drugs that provide new strategies to improve the effectiveness of cancer treatment. In our review, we summarize the current association between ANRIL and miRNAs in various cancers., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

As lncRNAs have increasingly been investigated, they are no longer simply defined as RNAs with no transcription capability. Studies have identified significant associations between the abnormal expression of lncRNAs and human diseases, particularly the mechanisms by which lncRNAs play a part in cancers, which are of considerable attention to researchers. As a result of the complex spatial structure, the mechanisms of interaction of lncRNAs in cancer cells are also complicated and diversified. Among a series of lncRNAs, TUG1, which is now considered to be a very high-value lncRNA, has recently been identified to express abnormally in some malignancies, leading to different alterations in cancer cells proliferation, migration, invasion, apoptosis, and drug resistance, and hence promoting or inhibiting cancer progression. Current studies have implicitly indicated that TUG1 can be used as a therapeutic target for human cancers. However, the biological functions of TUG1 have been studied for a short period of time, and the complete molecular mechanism still needs to be clarified. Accordingly, this review focuses on the principal molecular mechanisms of TUG1 in human cancers and the specific mechanisms of action in different cancer development processes based on existing studies., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Among all cancers in the world, the incidence rate of digestive system neoplasms accounts for about 25%, while the mortality rate accounts for about 35%. Difficulty in detecting early digestive system cancers and its poor prognosis are the two main reasons for the high mortality rate. Understanding of the basic cellular processes is of significance and autophagy is one of these processes. Considering the importance of autophagy in pathological state functions, the mechanism of autophagy was initially carried out. In this paper, we will review the molecular mechanisms and biological functions of autophagy-associated ncRNAs in different types of digestive system cancers. Autophagy is a process that supports nutrient cycling and metabolic adaptation accomplished through multi-step lysosomal degradation. It has been suggested that autophagy has a dual role in cancer, which limits tumorigenesis in some stages but promotes tumor progression in others. NcRNAs are also shown to modulate cellular autophagy and thus affect the development of digestive system neoplasms. More and more evidence suggests that the regulation of autophagy by ncRNAs plays a complex role in cancer initiation, progression, metastasis, recurrence, and treatment resistance, which might make ncRNAs therapeutic targets for digestive system neoplasms. While miRNAs participate mainly in post-transcriptional regulation, lncRNAs, and circRNAs usually serve as molecular sponges that have more diverse regulatory functions., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Despite advanced clinical treatment, the mortality rate of cancer patients is high. Recent studies have linked the development of cancer to inflammation. Many cancers are exacerbated by the emergence of inflammatory responses, and non-coding RNAs play an important role in inflammation. Non-coding RNAs include microRNAs, circular RNAs, long-chain noncoding RNAs, etc. The non-coding RNA regulatory network composed of microRNAs, circular RNAs and long-chain non-coding RNAs is involved in the regulatory process of multiple gene expression. They can act on various signaling pathways, such as wnt/β-catenin, nuclear factorkappa B, phosphatidylinositol 3 kinase/ AKT, mitogen-activated protein kinase, and so on. These signaling pathways can control the occurrence of inflammatory response to some extent, such as regulating the expression of inflammatory cytokines (such as interleukin-6, interferongamma, tumor necrosis factor-α, and so on), making them upregulated or down-regulated. Therefore, it is important to study the role of non-coding RNAs in inflammation to contribute to the future of cancer., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

CircRNA is stable due to its ring structure and is abundant in humans, which not only exists in various tissues and biofluids steadily but also plays a significant role in the physiology and pathology of human beings. CircPVT1, an endogenous circRNA, has recently been identified from the PVT1 gene located in the cancer risk region 8q24. CircPVT1 is reported to be highly expressed in many different tumors, where it affects tumor cell proliferation, apoptosis, invasion, and migration. We summarize the biosynthesis and biological functions of circPVT1 and analyze the relationship between circPVT1 and tumors as well as its significance to tumors. Further, it's noteworthy for the diagnosis, treatment, and prognosis of cancer patients. Therefore, circPVT1 is likely to become an innovative tumor marker., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Chronic myelogenous leukemia (CML) is a malignant myeloproliferative disease. According to the American Cancer Society's 2021 cancer data report, new cases of CML account for about 15% of all leukemias. CML is generally divided into three stages: chronic phase, accelerated phase, and blast phase. Nearly 90% of patients are diagnosed as a chronic phase. Allogeneic stem cell transplantation and chemotherapeutic drugs, such as interferon IFN-α were used as the earliest treatments for CML. However, they could generate obvious side effects, and scientists had to seek new treatments for CML. A new era of targeted therapy for CML began with the introduction of imatinib, the first-generation BCR-ABL kinase inhibitor. However, the ensuing drug resistance and mutant strains led by T315I limited the further use of imatinib. With the continuous advancement of research, tyrosine kinase inhibitors (TKI) and BCR-ABL protein degraders with novel structures and therapeutic mechanisms have been discovered. From biological macromolecules to classical target protein inhibitors, a growing number of compounds are being developed to treat chronic myelogenous leukemia. In this review, we focus on summarizing the current situation of a series of candidate small-molecule drugs in CML therapy, including TKIs and BCR-ABL protein degrader. The examples provided herein describe the pharmacology activity of small-molecule drugs. These drugs will provide new enlightenment for future treatment directions., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

MiRNAs are confirmed to be a kind of short and eminently conserved noncoding RNAs, which regulate gene expression at the post-transcriptional level via binding to the 3'- untranslated region (3'-UTR) of targeting multiple target messenger RNAs. Recently, growing evidence stresses the point that they play a crucial role in a variety of pathological processes, including human cancers. Dysregulated miRNAs act as oncogenes or tumor suppressor genes in many cancer types. Among them, we noticed that miR-122 has been widely reported to significantly influence carcinogenicity in a variety of tumors by regulating target genes and signaling pathways. Here, we focused on the expression of miR-122 in regulatory mechanisms and tumor biological processes. We also discussed the effects of miR-122 dysregulation in various types of human malignancies and the potential to develop new molecular miR-122-targeted therapies. The present review suggests that miR-122 may be a potentially useful cancer diagnosis and treatment biomarker. More clinical diagnoses need to be further launched in the future. A promising direction to improve the outcomes for cancer patients will likely combine miR-122 with other traditional tumor biomarkers., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Hepatocellular carcinoma is the sixth most common tumor and the third leading cause of cancer death worldwide. It ranks fourth in the spectrum of malignant tumor incidence and second in the order of death from major malignant tumors in China. Hepatocellular carcinoma is a complex ecosystem containing non-tumor cells (mainly immune-related cells), and its immunotherapy can stimulate the recognition of specific tumor antigens, inhibit the proliferation of cancer cells, and produce over-memory lymphocytes, which can prevent recurrence. So, immunotherapy of hepatocellular carcinoma is increasingly becoming a research hotspot in liver cancer treatment. With the intensive research in recent years, great progress has been made in immunotherapy for hepatocellular carcinoma, including immune checkpoint inhibitors, pericyte therapy, vaccination, and antiviral therapy. In addition, the study found that the therapeutic effect of combination therapy was enhanced compared to monotherapy. This review summarizes the most prominent immunotherapies currently available for the clinical treatment of patients with HCC and the main opportunities and challenges facing HCC research., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

MicroRNAs (miRNAs) are small non-coding RNAs 19-25 nucleotides in size involved in gene regulation and diverse processes in tumor cells. Abnormal expression of miRNAs is closely related to carcinogenesis. MiR-96 is a salient cancer-related miRNA in a variety of tumors. Recent evidence indicates that miR-96 has been observed to be wrapped in exosome and associated with drug resistance or radio-chemosensitivity in cancers. miR-96 is also inextricably linked with the competing endogenous RNAs (ceRNAs) in cancers. Notably, miR-96 plays both a tumor suppressor role and plays a carcinogenic role in the same cancers. This review summarizes the critical role of cancer-related miR-96 in drug resistance or radio-chemosensitivity and ceRNA mechanisms of miR-96 in cancer. And we innovatively propose that miR-96 has a yin-yang effect in cancers. Based on these several major roles of miR-96 in cancer as described above, we speculate that the abnormal expression of miR-96 is likely to be novel potential therapeutic targets in cancers. It is expected to solve the treatment problems such as low chemoradiotherapy sensitivity, poor prognosis quality of life and easy recurrence in cancer patients., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Gastric cancer is one of the most common and highest mortality rate cancers in the world. Exosomes are vesicles secreted by cells carrying different types of molecules, such as protein and RNA. Numerous studies have confirmed that exosomes are involved in various stages of the occurrence and development of gastric cancer and play an important role. With the gradual development, exosomes have been widely employed in the diagnosis and treatment of gastric cancer. In this review, we have provided a basic overview of exosome, and discussed the role of exosome in the occurrence, proliferation, invasion, metastasis, and drug resistance in gastric cancer. In addition, we have emphasized the bright development prospect of exosome in the diagnosis and treatment of gastric cancer. The data on the discovery, diagnosis, treatment, and prognosis of gastric cancer are not particularly optimistic, but the discovery of exosome, applied in diagnosis and treatment, provides a new and effective way to improve the survival rate of patients with gastric cancer., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

The article has been withdrawn at the request of the authors of the journal Mini-reviews in Medicinal Chemistry due to incoherent content., Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused., The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policiesmain. php., Bentham Science Disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript, the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net)

Multi-drug resistance (MDR) is characterized by the resistance of tumor cells to some antitumor drugs with different structures and mechanisms after the use of a single chemotherapy drug or even the first use of the drug. Notably, MDR has become the largest obstacle to the success of gastric cancer chemotherapies. Non-coding RNAs are defined as a class of RNAs that do not have the ability to code proteins. They are widely involved in important biological functions in life activities. Multiple lines of evidence demonstrated that ncRNAs are closely related to human cancers, including gastric cancer. However, the relationship between ncRNAs and MDR in gastric cancer has been reported, yet the mechanisms are not fully clarified. Therefore, in this review, we systematically summarized the detailed molecular mechanisms of lncRNAs (long noncoding RNAs) and miRNAs (microRNAs) associated with MDR in gastric cancer. Additionally, we speculate that the abnormal expression of ncRNAs is likely to be a novel potential therapeutic target reversing MDR for gastric cancer. Future therapeutics for gastric cancer will most likely be based on noncoding RNAs (ncRNAs) that regulate MDR-related genes., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Gastric cancer (GC), one of the common clinical malignant tumors of the digestive system, is the fourth most commonly diagnosed cancer and the second lethal cancer worldwide and has the characteristics of high metastasis, fatality, and recurrence rate. This research was conducted to investigate the role and mechanism of miR-4295 in gastric cancer., Methods: The expression capacity of miR-4295 was determined in gastric cancer tissues and its normal tissues by qRT-PCR. PTEN expression level was detected by western blot. SGC-7901 and MGC-803 cell lines were cultured and transfected with miR-4295 or its inhibitor. The effects of miR-4295 on cell proliferation, colony formation, migration, and invasion in vitro were investigated. The mutual effect between miR-4295 and PTEN in 293T cells was explored by luciferase reporter gene assays., Results: The results showed that miR-4295 expression was higher in gastric cancer tissues and cell lines, and the miR-4295 level was significantly negatively associated with the tumor size and distal metastasis of gastric cancer. Notably, up-regulated miR-4295 promoted cell proliferation, migration and invasion in vitro, whereas it led to contrary effects while down-regulating miR-4295 expression. Further mechanism studies displayed that miR-4295 could directly fasten the PTEN 3'UTR and dramatically decrease the level of PTEN in vitro., Conclusion: The findings revealed that miR-4295 could promote gastric cancer cell proliferation, migration and invasion, which might be attributed to targeting PTEN. Our study suggested that miR-4295 might be a potential therapeutic target for gastric cancer., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Hepatocellular carcinoma (HCC) is a common type of cancer with a high mortality rate and is usually detected at the middle or late stage, missing the optimal treatment period. The current study aims to identify potential long non-coding RNA (lncRNAs) biomarkers that contribute to the diagnosis and prognosis of HCC., Methods: The differentially expressed lncRNAs (DElncRNAs) in HCC patients were detected from the Cancer Genome Atlas (TCGA) dataset. LncRNAs signature was screened by LASSO regression, univariate, and multivariate Cox regression. The models for predicting diagnosis and prognosis were established, respectively. The prognostic model was evaluated by Kaplan-Meier survival curve receiver operating characteristic (ROC) curve and stratified analysis. The diagnostic model was validated by ROC. The lncRNAs signature was further demonstrated by functional enrichment analysis., Results: We found the 13-lncRNAs signature that had a good performance in predicting prognosis and could help to improve the value of diagnosis. In the training set, testing set, and entire cohort, the low-risk group had longer survival than the high-risk group (median OS: 3124 vs. 649 days, 2456 vs. 770 days and 3124 vs. 755 days). It performed well in 1-, 3-, and 5-year survival prediction. 13-lncRNAs-based risk score, age, and race were good predictors of prognosis. The AUC of diagnosis was 0.9487, 0.9265, and 0.9376, respectively. Meanwhile, the 13-lncRNAs were involved in important pathways, including the cell cycle and multiple metabolic pathways., Conclusion: In our study, the 13-lncRNAs signature may be a potential marker for the prognosis of HCC and improve the diagnosis., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)