LncRNA LINC00511 plays an oncogenic role in lung adenocarcinoma by regulating PKM2 expression via sponging miR‐625‐5p

Abstract

Background Lung adenocarcinoma (LAC) is the most prominent histological subtype of non‐small cell lung cancer (NSCLC) with a high rate of mortality and metastasis. Accumulating evidence has shown that long non‐coding RNAs (lncRNAs) play malfunctioning roles in the development of human tumors. Hence, this study aimed to determine the biological function of LINC00511 in LAC and to provide a novel diagnostic and therapeutic target for it. Methods LINC00511 expression in LAC tissues and cell lines (H1299 and A549) were detected by real time‐polymerase chain reaction (RT‐qPCR). Cell counting kit‐8 (CCK‐8) assay was employed to analyze cell proliferative ability. Cell metastasis change was measured using transwell assay. Moreover, we revealed a novel target gene of LINC00511 and elucidated the underlying competitive endogenous RNA regulatory mechanism in LAC cells. Results Data from our study demonstrated that LINC00511 expression was increased in LAC tissues and cells in comparison to their corresponding controls. Moreover, overexpression of LINC00511 indicated the poor prognosis of LAC patients. Overexpression of LINC00511 promoted proliferation, invasion and migration capacities of LAC cells. Moreover, LINC00511 promoted LAC progression via serving as a sponge of miR‐625‐5p and regulating PKM2 expression. Conclusions The present study showed that LINC00511 was involved in LAC progression by targeting miR‐625‐5p/PKM2, indicating that LINC00511/miR‐625‐5p/PKM2 may function as promising therapeutic targets for LAC.

SFPQ promotes an oncogenic transcriptomic state in melanoma

“…To this end, publicly available Ago2-CLIP data [ 32 ] was analysed to identify miRNAs that interact with LINC00511 and miR-625-5p identified as the top interactor (Fig. 4a ), an observation supported by several recent articles demonstrating that LINC00511 directly sponges miR-625-5p in renal, gastric and lung cancer [ 33 – 35 ]. To investigate if LINC00511 is functioning to sponge miR-625-5p in melanoma, LINC00511 was knocked down in A2058 cells, as described above, and miR-625-5p expression analysed via miRCURY LNA miRNA PCR Assay.…”

GAS6-AS1 Overexpression Increases GIMAP6 Expression and Inhibits Lung Adenocarcinoma Progression by Sponging miR-24-3p

“…Previous studies have demonstrated that lncRNAs play a vital role in inhibiting oncogenes and preventing the occurrence of malignant tumors ( 8 , 9 ). Several lncRNAs are aberrantly expressed in LUAD, leading to tumor inhibition or carcinogenicity depending on different mechanisms, including sponging and post-transcriptional regulation ( 10 – 13 ).…”

Crucial Roles of miR-625 in Human Cancer

“…In malignant pleural mesothelioma (MPM) (34,35) and thyroid cancer (TC) (36,37), miR-625 was found to be upregulated. It is downregulated in bladder cancer (38), nasopharyngeal carcinoma (NPC) (39), lung cancer (40)(41)(42)(43)(44)(45)(46), HCC (47), cervical cancer (CC) (48,49), osteosarcoma (50), melanoma (51)(52)(53)(54), laryngeal squamous cell carcinoma (LSCC) (55), acute myeloid leukemia (AML) (56), BC (57)(58)(59), glioma (60,61), esophageal cancer (EC) (62)(63)(64), clear cell renal cell carcinoma (65), GC (66)(67)(68)(69)(70), and pancreatic ductal adenocarcinoma (PDAC) (71). In colorectal cancer (CRC), the expression of miR-625 seems to vary, being either high or low.…”

“…Lung adenocarcinoma (LAC) is the most common histological subtype of NSCLC (88). Xue and Yang et al reported that miR-625 was involved in the process by which lncRNAs promoted the progression of LAC (45,46). Interestingly, miR-625 shows obvious antiinflammatory effect in both lung injury model and asthma model, through completely different molecular mechanisms (89,90).…”

“…In LAC, ccRCC, and GC, LINC00511 exerts carcinogenic effects by sponging miR-625. Members of the LINC00511/miR-625-5p/PKM2 axis may be helpful therapeutic targets for LAC (45).…”