MicroRNA‑150 suppresses p27^Kip1 expression and promotes cell proliferation in HeLa human cervical cancer cells

Abstract

MicroRNAs (miRNAs) exert critical roles in the majority of biological and pathological processes. Recent studies have associated miR-150 with a number of different cancer types. However, little is known about miR-150 targets in cervical cancer. In the present study, the HeLa human cervical cancer cell line was transfected with hsa-miR-150-5p mimics, hsa-miR-150-5p inhibitors or miRNA controls. miR-150 was predicted to bind the 3'untranslated region (3'UTR) of the CDKN1B gene, which encodes the cyclin-dependent kinase inhibitor 1B (p27 Kip1). The direct binding between miR-150 and the 3'UTR of CDKN1B was confirmed using dual-luciferase reporter assays. The effects of miR-150 on CDKN1B mRNA expression, p27 Kip1 protein expression, cell cycle and cell proliferation were determined using reverse-transcription quantitative PCR, western blot analysis, flow cytometry and WST-8 assays, respectively. miR-150 was demonstrated to directly target the 3'UTR of CDKN1B in transfected HeLa cells. The expression of CDKN1B mRNA and p27 Kip1 protein was reduced by miR-150 mimics, and increased by miR-150 inhibitors. Moreover, the overexpression of miR-150 promoted cell cycle progression from the G0/G1 to the S phase and led to a significant increase in HeLa cell proliferation. The results of the present study indicated that miR-150 promotes HeLa cell cycle progression and proliferation via the suppression of p27 Kip1 expression.

CKS1B as a potential target for prognostic assessment and intervention in pancreatic cancer and its role in abnormal proliferation and cellular phenotype through mediation of cell cycle signaling pathways

“…It is important to note that CKS1B can also be negatively regulated by other miRNAs. 24 For example, miR-520h has been shown to inhibit CKS1B overexpression, mitigating the inhibitory effects on PACA-2 cells’ viability, migration, as well as invasion following LINC00657 knockdown. Furthermore, miR-1258 has been identified as another miRNA that negatively regulates CKS1B expression, leading to the inhibition of colorectal cancer cell proliferation, migration, and tumorigenicity.…”

“…Numerous miRNAs with deleterious regulatory functions are situated upstream of mRNAs and actively participate in the processes of tumorigenesis and tumor development. [22][23][24] In this study, a specific miRNA, has-miR-150-5p, was identified through database analysis as a negative regulator of CKS1B. This miRNA has previously been linked to the advancement of nasopharyngeal and cervical cancers by suppressing PYCR1 and p27 Kip1's expression.…”

The prognostic value of MicroRNAs associated with fatty acid metabolism in head and neck squamous cell carcinoma

“…In addition, a screening of differentially expressed miRNAs in gastric cancer showed hsa-miR-148a-3p, hsa-miR-148b-3p, and hsa-miR-363-3p as having the greatest number of target genes, three microRNAs were significantly overrepresented in numerous cancer-related pathways, including the “Wnt signaling route,” the “MAPK signaling pathway,” and the “Jak-STAT signaling pathway” ( Luo et al, 2015 ). Overexpression of hsa-miR-150-5p accelerated the passage of human cervical cancer cells from G0/G1 to S phase, resulting in a considerable increase in cell proliferation ( Oboshi et al, 2020 ). In addition, the overexpression of hsa-miR-150-5p was linked to an increased risk of Chronic lymphocytic leukemia ( Casabonne et al, 2020 ).…”

Associated with Immune Function, miR-150-5p is a Favorable Biomarker for Head and Neck Cancer Patients

“…The GSEA analysis also revealed that several oncogenic pathways were down-regulated in the case of high expression of miR-150. Although miR-150-5p acts as oncogene in some cancers [6,[36][37][38], miR-150-5p has mostly been show to play an anti-tumor role in cancer [5,[39][40][41][42][43][44][45][46][47]. The different roles of miR-150-5p in different studies and cancer types might depend on the target gene it regulates.…”