Oncogenic microRNA-142-3p is associated with cellular migration, proliferation and apoptosis in renal cell carcinoma

Abstract

Abstract. MicroRNAs (miRNAs/miRs) serve an important role in the regulation of carcinogenic pathways. RCC is the most prevalent kidney cancer that occurs in adults. miRNAs have gained increasing attention due to their association with RCC tumorigenesis, serving as biomarkers for early detection and progression monitoring, and as potential targets for molecular therapy. Upregulation of miRNA-142-3p has been previously identified in RCC tissues by microarray profile, however, its expression and function in RCC have not yet been validated. In the present study, quantitative polymerase chain reaction was performed to quantify the relative expression of miR-142-3p in 53 paired RCC and adjacent normal tissues. Furthermore, wound healing, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry assays were performed to analyze the impacts of miR-142-3p on cellular migration, proliferation and apoptosis. The results demonstrated that miR-142-3p was significantly upregulated in RCC tissues compared with adjacent normal tissues. Downregulation of miR-142-3p, induced by chemically synthesized miR-142-3p inhibitor, significantly suppressed cell migration and proliferation, and promoted cell apoptosis in 786-O and ACHN cells, supporting the theory that miR-142-3p may function as an oncogene in RCC. The potential clinical significance of miR-142-3p, as a biomarker and therapeutic target, provides rationale for further investigation into the miR-142-3p-mediated molecular pathway and how it is associated with RCC development.

miR-142-3p Suppresses Cell Growth by Targeting CDK4 in Colorectal Cancer

“…Most recent, miR-142-3p has been reported to be associated with several types of cancer. MiR-142-3p was significantly upregulated in renal cell carcinoma and miR-142-3p inhibitor could significantly suppressed cell migration and proliferation, and promoted cell apoptosis in 786-O and ACHN cells [30]; miR-142-3p was down-regulated in both cancer cell lines and cancer specimens and miR-142-3p overexpression suppressed proliferation by leading cell cycle arrest in G2/M [31]; miR-142-3p was downregulated in hepatocellular carcinoma (HCC) tissues and the overexpression of miR-142-3p inhibited aerobic glycolysis and thus proliferation of HCC cells by targeting lactate dehydrogenase A (LDHA) [32]; miR-142-3p was significantly lower in ovarian cancer tissues and cell lines and Ectopic expression of miR-142-3p significantly inhibited the proliferation of ovarian cancer cells by targeting sirtuin 1 (SIRT1) and increased the sensitivity of SKOV3/DDP cells to cisplatin [33]; miR-142-3p was markedly downregulated in gastric cancer tissues and could inhibit the proliferation, invasion and migration of gastric cancer cells [34]; miR-142-3p inhibited proliferation and invasion in HeLa and SiHa cells by targeting frizzled 7 receptor [FZD7] [35]; miR-142-3p miR-142-3p downregulated MGMT expression and also sensitizedGlioblastoma multiforme [GBM] cells to alkylating drugs [36]; miR-142-3p overexpression increased PI3K, Akt, and mTOR phosphorylation by targeting High mobility group box-1 [HMGB1] in NSCLS cells [37]. According to CRC, three studies have suggested that miR-142-3p is involved in CRC development.…”

Extracellular vesicle secretion of miR‐142‐3p from lung adenocarcinoma cells induces tumor promoting changes in the stroma through cell‐cell communication

“…34,[49][50][51] In renal cell carcinoma tissue miR-142-3p was found to be elevated compared to adjacent normal tissue and functioned as an oncogenic miRNA, as when miR-142-3p was inhibited proliferation and migration were reduced and apoptosis was promoted. 51 In nasopharyngeal cancer miR-142-3p inhibition lead to a decrease in proliferation and cell cycle progression in vitro and suppressed tumor growth in mouse models. 49 In T-Cell acute lymphoblastic leukemia, miR-142-3p at high levels reduced cyclic adenosine monophosphate (cAMP) and protein kinase This suggests that miR-142-3p can serve as both tumor suppressor and oncogene depending on the cell type in which it is present.…”

miR-142 inhibits the migration and invasion of glioma by targeting Rac1

“…In addition, serum miR-142 is associated with early relapse in operable lung adenocarcinoma patients (23). However, the expression of miR-142 is overexpressed in nasopharyngeal carcinoma (24), testicular (25), and head and neck cancer (26), esophageal squamous cell (27) and renal cell carcinoma (28). miR-142 suppresses SOCS6 expression and promotes cell proliferation in nasopharyngeal carcinoma (24).…”

“…miR-142 suppresses SOCS6 expression and promotes cell proliferation in nasopharyngeal carcinoma (24). Oncogenic miR-142 is associated with cellular migration, proliferation and apoptosis in renal cell carcinoma (28). Therefore, it is suggested that the functional significance of miR-142 in tumorigenesis and progression is cancer-type specific.…”