MicroRNAs (miRNAs) are small non‑coding RNAs that serve key roles in cell proliferation, migration, invasion and apoptosis by regulating gene expression. In malignant tumors, miRNA‑122 serves either as a tumor suppressor or oncogene, influencing tumor progression via downstream gene targeting. However, the precise role of miRNA‑122 in cancer remains unclear. miRNA‑122 is a potential biomarker and modulator of radiotherapy and chemotherapy. The present review aimed to summarize the roles of miRNA‑122 in cancer, its potential as a biomarker for diagnosis and prognosis and its implications in cancer therapy, including radiotherapy and chemotherapy, alongside strategies for systemic delivery.

The N-myc downstream regulated gene family (NDRGs) includes four members: NDRG1, NDRG2, NDRG3, and NDRG4. These members exhibit 53-65% amino acid identity. The role of NDRGs in tumor growth and metastasis appears to be tumor- and context-dependent. While many studies have reported that these family members have tumor suppressive roles, recent studies have demonstrated that NDRGs, particularly NDRG1 and NDRG2, function as oncogenes, promoting tumor growth and metastasis. Additionally, NDRGs are involved in regulating different signaling pathways and exhibit diverse cellular functions in breast cancers. In this review, we comprehensively outline the oncogenic and tumor suppressor roles of the NDRG family members in breast cancer, examining evidence from in vitro and in vivo breast cancer models as well as tumor tissues from breast cancer patients. We also present analyses of publicly available genomic and transcriptomic data from multiple independent cohorts of breast cancer patients.

Long non-coding RNA papillary thyroid carcinoma susceptibility candidate 3 (LncRNA PTCSC3) is located on human chromosome 14q13.3. PTCSC3 functions as a tumor suppressor lncRNA to regulate essential cellular processes such as apoptosis, cell proliferation, migration, invasion, angiogenesis, and epithelial-to-mesenchymal transition. PTCSC3 is also involved in the regulation of the Wnt/β-catenin signaling pathway, aerobic glycolysis, and p53 pathways. Downregulation of PTCSC3 has been associated with an increased risk of many tumors such as thyroid, gastric, laryngeal, breast, cervical, oral, lung, and glioma cancers. In addition, dysregulation of PTCSC3 has been reported in non-cancerous disorders notably osteoporosis and periodontitis. However, a number of single nucleotide polymorphisms at PTCSC3 have been linked to a higher risk of human diseases. This literature review summarizes the diagnostic, prognostic, and the clinical value of abnormal expression of PTCSC3 in cancerous and non-cancerous disorders and comprehensively analyzes potential molecular regulatory mechanism related to PTCSC3, which is expected to provide clear guidance for future PTCSC3 research.

Histone alterations are a hallmark of kidney cancer. Histone acetylation modification mediated by bromodomain proteins (BRD) has been indicated to be related to a variety of cancer types and several targeted inhibitors have been proven to be promising modalities for cancer adjuvant therapy. As renal cell carcinoma (RCC) is not sensitive to radiotherapy or chemotherapy, the exploration of effective adjuvant therapies remains an important research direction for advanced RCC. At present, studies on bromodomain family proteins in RCC are limited and the roles of bromodomain family proteins in RCC have remained to be fully elucidated. The present review discussed the role of bromodomain family proteins in RCC, aiming to explore possible potential therapeutic targets of BRD‑related drugs in this type of cancer.

Long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) is a lncRNA located at the DLK1-MEG3 site of human chromosome 14q32.3. The expression of MEG3 in various tumors is substantially lower than that in normal adjacent tissues, and deletion of MEG3 expression is involved in the occurrence of many tumors. The high expression of MEG3 could inhibit the occurrence and development of tumors through several mechanisms, which has become a research hotspot in recent years. As a member of tumor suppressor lncRNAs, MEG3 is expected to be a new target for tumor diagnosis and treatment. This review discusses the molecular mechanisms of MEG3 in different tumors and future challenges for the diagnosis and treatment of cancers through MEG3.

The investigation of tumor microenvironment (TME) is essential to better characterize the complex cellular crosstalk and to identify important immunological phenotypes and biomarkers. The niche is a crucial contributor to neoplasm initiation, maintenance and progression. Therefore, a deeper analysis of tumor surroundings could improve cancer diagnosis, prognosis and assertive treatment. Thus, the WNT family exerts a critical action in tumorigenesis of different types of neoplasms due to dysregulations in the TME. WNT5A, an evolutionary WNT member, is involved in several cellular and physiopathological processes, in addition to tissue homeostasis. The WNT5A protein exerts paradoxical effects while acting as both an oncogene or tumor suppressor by regulating several non-canonical signaling pathways, and consequently interfering in cell growth, cytoskeletal remodeling, migration and invasiveness. This review focuses on a thorough characterization of the role of WNT5A in neoplastic transformation and progression, which may help to understand the prognostic potentiality of WNT5A and its features as a therapeutic target in several cancers. Additionally, we herein summarized novel findings on the mechanisms by which WNT5A might favor tumorigenesis or suppression of cancer progression and discussed the recently developed treatment strategies using WNT5A as a protagonist.

Wingless-related integration site (Wnt) signaling is one of the main oncogenic pathways in different malignancies. Therefore, targeting this pathway has been considered an exciting strategy in cancer treatment. Porcn is among the central enzymes in this pathway that has recently been considered for cancer-targeted therapy. As a membrane-bound O-acyltransferase, Porcn plays a critical role in wnt ligand palmitoylation and its subsequent secretion. In addition to Porcn\'s role in stem cell signaling and differentiation, recent findings have shown its role in developing and progressing colorectal, pancreatic, liver, head, and neck cancers. Developed small molecule inhibitors have also opened a promising window toward cancer treatment strategies. In this review, the structure and biological role of Porcn in different cancer-related signaling pathways and inhibitors used for inhibiting this enzyme are discussed.

Gastrointestinal (GI) cancer is associated with a group of cancers affecting the organs in the GI tract, with a high incidence and mortality rate. This type of cancer development involves a series of molecular events that arise by the dysregulation of gene expressions and microRNAs (miRNAs).
This mini-review focuses on elucidating the mechanism of tumor suppressor miRNA-mediated oncogenic gene silencing, which may contribute to a better understanding of miRNA-mediated gene expression regulation of cell cycle, proliferation, invasion, and apoptosis in GI cancers. In this review, the biological significance of tumor suppressor miRNAs involved in gastrointestinal cancers is briefly explained.
The articles were searched with the keywords \'miRNA\', \'gastrointestinal cancers\', \'esophageal cancer\', \'gastric cancer\', \'colorectal cancer\', \'pancreatic cancer\', \'liver cancer\', and \'gall bladder cancer\' from the Google Scholar and PubMed databases. A total of 71 research and review articles have been collected and referred for this study.
This review summarises recent research enhancing the effectiveness of miRNAs as novel prognostic, diagnostic, and therapeutic markers for GI cancer treatment strategies. The expression pattern of various miRNAs has been dysregulated in GI cancers, which are associated with proliferation, cell cycle regulation, apoptosis, migration, and invasion.
The role of tumor suppressor miRNAs in the negative regulation of oncogenic gene expression was thoroughly explained in this review. Its potential role as a microRNA therapeutic candidate is also discussed. Profiling and regulating tumor suppressor miRNA expression in gastrointestinal cancers using miRNA mimics could be used as a prognostic, diagnostic, and therapeutic marker, as well as an elucidating molecular therapeutic approach to tumor suppression.

The dysregulation of the ubiquitin‑proteasome system will result in the abnormal accumulation and dysfunction of proteins, thus leading to severe diseases. Seven in absentia homolog 1 (Siah1), an E3 ubiquitin ligase, has attracted wide attention due to its varied functions in physiological and pathological conditions, and the numerous newly discovered Siah1 substrates. In cancer and nervous system diseases, the functions of Siah1 as a promoter or a suppressor of diseases are related to the change in cellular microenvironment and subcellular localization. At the same time, complex upstream regulations make Siah1 different from other E3 ubiquitin ligases. Understanding the molecular mechanism of Siah1 will help the study of various signaling pathways and benefit the therapeutic strategy of human diseases (e.g., cancer and nervous system diseases). In the present review, the functions and regulations of Siah1 are described. Moreover, novel substrates of Siah1 discovered in recent studies will be highlighted in cancer and nervous system diseases, providing ideas for future research and clinical targeted therapies using Siah1.

MicroRNAs(miRNAs) are small non-coding RNAs which have a critical role in various biological processes via direct binding and post-transcriptionally regulating targeted genes expression. More than one-half of human genes were regulated by miRNAs and their aberrant expression was detected in various human diseases, including cancers. miRNA-338 is a new identified miRNA and increasing evidence show that miRNA-338 participates in the progression of lots of cancers, such as lung cancer, hepatocellular cancer, breast cancer, glioma, and so on. Although a range of targets and signaling pathways such as MACC1 and Wnt/β-catenin signaling pathway were illustrated to be regulated by miRNA-338, which functions in tumor progression are still ambiguous and the underlying molecular mechanisms are also unclear. Herein, we reviewed the latest studies in miRNA-338 and summarized its roles in different type of human tumors, which might provide us new idea for further investigations and potential targeted therapy.