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.

Long non-coding RNAs have emerged as important players in cancer biology. Increasing evidence has uncovered their potency in improving cancer management as they can be used as a credible prognostic and diagnostic biomarker. Recently, DARS-AS1 has gained significant attention for its involvement in facilitating tumor progression. So far, numerous research has been reported its upregulation in different malignancies of human body systems and revealed its association with cancer hallmarks as well as clinicopathological characteristics. Importantly, targeting DARS-AS1 holds promise in cancer therapy. In the current study, we provide an in-depth analysis of its expression status and explore the underlying mechanisms through which DARS-AS1 contributes to tumor initiation, growth, invasion, and metastasis. Additionally, we examine the correlation between DARS-AS1 expression and clinicopathological features of cancer patients, shedding light on its potential as a cancer biomarker. Furthermore, we discuss the therapeutic potential of targeting DARS-AS1 in cancer treatment, highlighting emerging strategies, such as RNA interference and small molecule inhibitors. Boosting the understanding of its functional role can open new avenues for precision medicine, thus resulting in better outcomes for cancer patients.

Melanocytic nevi (skin moles) have been regarded as a valuable example of cell senescence occurring in vivo. However, a study of induced nevi in a mouse model reported that the nevi were arrested by cell interactions rather than a cell-autonomous process like senescence, and that size distributions of cell nests within nevi could not be accounted for by a stochastic model of oncogene-induced senescence. Moreover, others reported that some molecular markers used to identify cell senescence in human nevi are also found in melanoma cells-not senescent. It has thus been questioned whether nevi really are senescent, with potential implications for melanoma diagnosis and therapy. Here I review these areas, along with the genetic, biological, and molecular evidence supporting senescence in nevi. In conclusion, there is strong evidence that cells of acquired human benign (banal) nevi are very largely senescent, though some must contain a minor non-senescent cell subpopulation. There is also persuasive evidence that this senescence is primarily induced by dysfunctional telomeres rather than directly oncogene-induced.

The transcription factor, known as basic leucine zipper ATF-like 3 (BATF3), is a crucial contributor to the development of conventional type 1 dendritic cells (cDC1), which is definitely required for priming CD8 + T cell-mediated immunity against intracellular pathogens and malignancies. In this respect, BATF3-dependent cDC1 can bring about immunological tolerance, an autoimmune response, graft immunity, and defense against infectious agents such as viruses, microbes, parasites, and fungi. Moreover, the important function of cDC1 in stimulating CD8 + T cells creates an excellent opportunity to develop a highly effective target for vaccination against intracellular pathogens and diseases. BATF3 has been clarified to control the development of CD8α+ and CD103+ DCs. The presence of BATF3-dependent cDC1 in the tumor microenvironment (TME) reinforces immunosurveillance and improves immunotherapy approaches, which can be beneficial for cancer immunotherapy. Additionally, BATF3 acts as a transcriptional inhibitor of Treg development by decreasing the expression of the transcription factor FOXP3. However, when overexpressed in CD8 + T cells, it can enhance their survival and facilitate their transition to a memory state. BATF3 induces Th9 cell differentiation by binding to the IL-9 promoter through a BATF3/IRF4 complex. One of the latest research findings is the oncogenic function of BATF3, which has been approved and illustrated in several biological processes of proliferation and invasion.

Prostate cancer is the leading cause of cancer‑related mortality among men worldwide. In particular, castration‑resistant prostate cancer presents a formidable clinical challenge and emphasizes the need to develop novel therapeutic strategies. Forkhead box M1 (FOXM1) is a multifaceted transcription factor that is implicated in the acquisition of the multiple cancer hallmark capabilities in prostate cancer cells, including sustaining proliferative signaling, resisting cell death and the activation of invasion and metastasis. Elevated FOXM1 expression is frequently observed in prostate cancer, and in particular, FOXM1 overexpression is closely associated with poor clinical outcomes in patients with prostate cancer. In the present review, recent advances in the understanding of the oncogenic role of deregulated FOXM1 expression in prostate cancer were highlighted. In addition, the molecular mechanisms by which FOXM1 regulates prostate cancer development and progression were described, thereby providing knowledge and a conceptual framework for FOXM1. The present review also provided valuable insight into the inherent challenges associated with translating biomedical knowledge into effective therapeutic strategies for prostate cancer.

Activating transcription factor 2 (ATF2) is a member of the leucine zipper family of DNA binding proteins that are responsible for regulating various genes that play an essential role in major biological and cellular functions. Since ATF2 plays a vital role in cellular proliferation and apoptosis, it is believed that it greatly affects the development of breast cancers. However, its exact role in breast cancer is incompletely understood. It remains a subject of debate, ambiguity, and continuous research. Several studies have suggested the role of ATF2 as an oncogene, promoting cellular proliferation and worsening the outcome of cancers. In contrast, other studies have postulated that ATF2 plays a tumor suppressive role in estrogen receptor-positive breast cancer. The ambiguity surrounding its role in breast cancer is the reason why there is an influx of recent studies and research in this area. In this narrative review, we investigate several studies that have been published about the role of ATF2 in breast cancer. We also explore studies that have examined the association between ATF2 and endocrine therapy resistance. ATF2 has been suggested to modulate estrogen receptor (ER) expression and activity, potentially affecting tamoxifen sensitivity in breast cancer cells. Therefore, the role of ATF2 in DNA repair mechanisms and drug resistance has been deeply explored in this review. Additionally, there are numerous ongoing clinical trials exploring the effect of targeting ATF2 pathways and mechanisms on the outcome of breast cancers, some of which we have discussed. The studies and clinical trials that are being conducted to understand the multifaceted role of ATF2 and its signaling pathways may provide valuable insight for developing efficient targeted therapeutic solutions to enhance the outcomes of breast cancer and overcome endocrine resistance. We suggest further research to elucidate the dual roles of ATF2 in breast cancer and potential therapeutic therapies for its treatment.

Research on Rab-like protein 1A (RBEL1A) in the past two decades highlighted the oncogenic properties of this gene. Despite the emerging evidence, its importance in cancer biology was underrated. This is the first RBEL1A critical review covering its discovery, biochemistry, physiological functions, and clinical insights. RBEL1A expression at the appropriate levels appears essential in normal cells and tissues to maintain chromosomal stability; however, its overexpression is linked to tumorigenesis. Furthermore, the upstream and downstream targets of the RBEL1A signaling pathways will be discussed. Mechanistically, RBEL1A promotes cell proliferation signals by enhancing the Erk1/2, Akt, c-Myc, and CDK pathways while blunting the apoptotic signals via inhibitions on p53, Rb, and caspase pathways. More importantly, this review covers the clinical relevance of RBEL1A in the cancer field, such as drug resistance and poor overall survival rate. Also, this review points out the bottle-necks of the RBEL1A research and its future research directions. It is becoming clear that RBEL1A could potentially serve as a valuable target of anticancer therapy. Genetic and pharmacological researches are expected to facilitate the identification and development of RBEL1A inhibitors as cancer therapeutics in the future, which could undoubtedly improve the management of human malignancy.

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.

Digestive system cancers are the leading cause of cancer‑related death worldwide due to their high morbidity and mortality rates. The current treatment methods include surgical treatment, chemotherapy, radiotherapy and endoscopic treatment, and the precisely targeted therapy of digestive system cancers requires to be further studied. The ubiquitin‑proteasome system is the main pathway for protein degradation in cells and the ubiquitin‑conjugating enzymes (E2s) have a decisive role in the specific selection of target proteins for degradation. The E2s have an important physiological role in digestive system cancers, which is related to the clinical tumor stage, differentiation degree and poor prognosis. Furthermore, they are involved in the physiological processes of digestive system tumor cell proliferation, migration, invasion, stemness, drug resistance and autophagy. In the present article, the progress and achievements of the E2s in gastric cancer, hepatocellular carcinoma, pancreatic cancer, colorectal cancer, intrahepatic cholangiocarcinoma, gallbladder cancer and esophageal squamous cell carcinoma were reviewed, which may provide early screening indicators and reliable therapeutic targets for digestive system cancers.

Long non-coding RNAs (lncRNAs) have more than 200 nucleotides and do not encode proteins. At the same time, they can regulate various biological functions and therefore play an essential role as oncogenes or tumor suppressors in human cancers. MAFG-AS1 is an antisense RNA of MAF BZIP Transcription Factor G (MAFG) located at chromosome 17q25.3 head-to-head with the MAFG encoding gene containing a transcript size of 1895 bp. Accumulating evidence shows that MAFG-AS1 is overexpressed in many cancers, functions as an oncogene, and is significantly associated with poor clinical characteristics and prognosis. In this review, we first discuss the recent literature regarding the role of MAFG-AS1 in different cancers as well as its diagnostic and prognostic values. Then we will provide insights into its biological functions, such as its role in cancer progression, competing endogenous RNA (ceRNA) activity, regulation of EMT, glycolysis, energy metabolism, transcription factors, proteasomal degradation, and signaling pathways.