LINC00941 promoted in vitro progression and glycolysis of laryngocarcinoma by upregulating PKM via activating the PI3K/AKT/mTOR signaling pathway

Abstract

Background LINC00941 has been proved to be related to various tumors, but its relationship with laryngocarcinoma remains vague. Methods LINC00941 expression in laryngocarcinoma tumor and laryngocarcinoma cells was determined by real time‐quantitative polymerase chain reaction (RT‐qPCR). Besides, the five‐year survival of laryngocarcinoma patients with different LINC00941 expression was analyzed with Kaplan–Meier survival analysis, and the clinical characteristics of laryngocarcinoma patients were also recorded. After transfection, cell viability, cell proliferation, apoptosis, cell cycle, migration, and invasion were detected by cell counting kit‐8 (CCK‐8), colony formation, flow cytometry, cell scratch, and Transwell assays, respectively. Glycolysis was assessed by the colorimetric method. Expressions of proliferation‐associated proteins, migration‐associated proteins, glycolysis‐associated proteins, and phosphatidylinositol 3‐kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signal pathway‐associated proteins were detected by Western blot. Results In laryngocarcinoma tumor tissues and cells, LINC00941 was highly expressed. High expression of LINC00941 decreased the 5‐year survival of laryngocarcinoma patients, and it was positively related to lymph node metastasis and clinical stages. LINC00941 overexpression decreased apoptosis but promoted cell viability, proliferation, cell‐cycle progression, migration, and invasion, and glucose consumption and lactate production in laryngocarcinoma cells. Moreover, LINC00941 overexpression elevated expressions of Ki‐67, PCNA, MMP2, N‐Cadherin, HK2, PFKFB4, and PKM, activated the PI3K/AKT/mTOR signal pathway but reduced E‐Cadherin expression, while LINC00941 silencing had the opposite effects. PKM overexpression reversed the effects of LINC00941 silencing on cellular and glycolytic phenotypes. Conclusion LINC00941 promoted in vitro progression and glycolysis of laryngocarcinoma cells by upregulating PKM via activating the PI3K/AKT/mTOR signaling pathway.

lncHUB2: aggregated and inferred knowledge about human and mouse lncRNAs

“…It was also identified that ATF3 transcription factor enhances LINC00941 expression. Additionally, LINC00941 was shown to promote glycolysis and laryngocarcinoma progression through the PI3K/AKT/mTOR signaling pathway and its upregulation of PKM ( 102 ).…”

Prediction of network pharmacology, molecular docking-based strategy, and vitro assays to determine potential pharmacological mechanism of Dioscoreae bulbiferae and Bruceae fructus against laryngocarcinoma

“…[ 38 ] PI3K-Akt is a unique master regulator of various cancers and can also regulate the occurrence and development of laryngeal cancer. [ 39 ] As a tumor promoter, the TNF signaling pathway plays an important role in regulating the occurrence and metastasis of tumors. [ 40 ] Studies have shown that by regulating the TNF signaling pathway, Protein Tyrosine Phosphatase Non-Receptor Type 2 is highly expressed in laryngeal cancer and can regulate the proliferation of laryngeal cancer.…”

LncRNA-MUF: A Novel Oncogenic Star with Potential as a Biological Marker and Therapeutic Target for Gastrointestinal Malignancies

“…This singular transcript feature of the gene highlights its unique molecular characteristics in GI cancer studies. Recently, a large number of studies have shown that it is involved in the progression of various tumors [27][28][29][30][31][32][33][34], particularly in GI malignancies [35][36][37][38][39][40][41][42][43][44][45][46][47]. Dysregulated expression of LINC00941 has been observed in GI tumors [35,43,44,46].…”