miR-143 inhibits cell proliferation by targeting autophagy-related 2B in non-small cell lung cancer H1299 cells

Abstract

microRNAs (miRNAs) are small, non‑coding RNAs involved in multiple biological pathways by regulating post-transcriptional gene expression. Previously, autophagy has been reported to suppress the progression of non-small cell lung cancer (NSCLC). However, how miRNAs regulate autophagy in NSCLC remains to be elucidated. In the present study, the autophagy gene, autophagy-related 2B (ATG2B), was identified as a novel target of miR-143. The overexpression of miR-143 was able to downregulate the expression of atg2b at the transcriptional and translational levels by direct binding to its 3' untranslated region. Cell proliferation was significantly inhibited by the ectopic expression of miR-143 in H1299 cells. Knockdown of ATG2B resulted in a similar phenotype, with the overexpression of miR-143 in NSCLC cells. Furthermore, knockdown of ATG2B and hexokinase 2, a key enzyme in glycolysis and another target of miR-143, co-ordinated to inhibit the proliferation of H1299 cells. The results of the present study demonstrated that miR-143 was a novel and important regulator of autophagy by targeting ATG2B and repression of gene expression in autophagy and high glycolysis had a coordinate effect in H1299 cells. These results suggested that ATG2B may be a new potential therapeutic target for NSCLC. Furthermore, it was implied that interrupting autophagy and glycolysis improves NSCLC therapy.

Human adipose mesenchymal stem cell-derived exosomal-miRNAs are critical factors for inducing anti-proliferation signalling to A2780 and SKOV-3 ovarian cancer cells

“…Member(s) of the hsa-miR-18114 and hsa-miR-29 families15 exhibit both anticancer and pro-cancer regulation under different clinical conditions, while members of hsa-miR-12616, hsa-miR-12917, hsa-miR-13618, hsa-miR-20419, hsa-miR-66320, hsa-miR-9921, hsa-miR-37822, hsa-miR-9223, and hsa-miR-40924 families are recognized as having anticancer properties under different clinical conditions. Families that contained at least one miRNA found in hAMSC-CM-derived exosomes reportedly exhibit antagonistic roles in numerous cancer types and include hsa-miR-48625, hsa-miR-10026, hsa-miR-10127, hsa-miR-12428, hsa-miR-128529, hsa-miR-13430, hsa-miR-13831, hsa-miR-13932, hsa-miR-14333, hsa-miR-18634, hsa-miR-19335, hsa-miR-20536, hsa-miR-22237, hsa-miR-33838, hsa-miR-33939, hsa-miR-42440, hsa-miR-12741, hsa-miR-2642, hsa-miR-10343, hsa-miR-10744, hsa-miR-12845, hsa-miR-14046, hsa-miR-14447, hsa-miR-15348, hsa-miR-19249, hsa-miR-21250, hsa-miR-21851, hsa-miR-2352, hsa-miR-2553, hsa-miR-37054, hsa-miR-37555, hsa-miR-38156, hsa-miR-41057, hsa-miR-4158, and hsa-miR-9359. These NGS data revealed an enriched miRNA population in hAMSC-CM-derived exosomes that are likely involved in the regulation of different types of cancer.…”

MiR-142-3p Overexpression Increases Chemo-Sensitivity of NSCLC by Inhibiting HMGB1-Mediated Autophagy

“…A recent study has revealed that miR-143 inhibits NSCLC cell proliferation by targeting the autophagy gene, autophagy-related 2B [45]. HMGB1 is present at increased levels in NSCLC patients [46].…”

Efficacy of Plasma microRNA-143 and microRNA-550a as Potential Diagnostic and Prognostic Biomarkers for Chronic Hepatitis and Hepatocellular Carcinoma in Egyptian Patients

“…Discussion miR-143 is located in the chromosome 5 with a mature length of 22 [10]. A previous study has revealed that miR-143 exhibited down-regulation in many cancers such as colorectal cancer [11], pancreatic cancer [12] and lung cancer [13] in which miR-143 acts as a tumor suppressor inhibiting cell proliferation and inducing tumor cell apoptosis thus hindering the development of cancer [10]. miR-143 was exploited in many cancers e.g.…”

“…On the other hand; this could also be explained by the hepatocyte destruction due to the HCC and hence higher level in the blood. Autophagy gene 2B (ATG2B) was found to be a possible target for miR-143, where miR-143 Overexpression is associated with down regulation of ATG2B [13]; thus decreasing the autophagy responsible for the cancer cell survival and inducing apoptosis [20].…”