The mechanism of LncRNA01977 in lung adenocarcinoma through the SDF-1/CXCR4 pathway

Abstract

Background: A significant correlation has been identified between lncRNA and tumor cell resistance, diagnosis, and prognosis. Although mRNA studies have dominated the field of non-coding RNA biology in tumorigenesis in recent years, long-chain non-coding RNA (the biological function) has also attracted increasing attention. However, the lncRNA associated with lung adenocarcinoma (LUAD) remains unexplored. This study used bioinformatics analysis to screen and identify LncRNA01977 as a key oncogenic driver of LUAD. Methods:The experiment was divided into blank serum group (normal serum medium) and lung compound low, medium and high dose groups (5%, 10%, 15% and 15% lung compound drug serum medium, respectively). Transwell invasion ability of A549 cells was detected, and Western blot tested A549 cells SDF-1 specific receptor CXCR4, and CXCR4 gene expression in A549 cells were determined by reverse transcription-polymerase chain reaction (RT-PCR). In addition, western blotting, MTT proliferation test, colony formation test and apoptosis detection techniques were used to explore the mechanism of LncRNA01977's effects on LUAD.Results: In vitro assays demonstrated that LncRNA01977 can significantly promote the progression of LUAD and that stromal cells in tumor microenvironment secrete chemokine CXCL12, also known as stromal derived factor-1 (SDF-1), and its receptor CXCR4 is low expressed in normal tissues and high expressed in LUAD tissues. Lung cancer patients with high expression of CXCR4 are more prone to metastasis.Conclusions: LncRNA01977 can be used as a new prognostic indicator of LUAD, and can help patients to find more effective target treatment options for LUAD.

Hepatocyte-targeted delivery using oleanolic acid-loaded liposomes for enhanced hepatocellular carcinoma therapy

“…, JNK/p38, MAPK, and PI3K/Akt/mTOR), thereby inhibiting tumor metastasis. 46,47 EMT is a fundamental process that has been implicated in tumor progression. 48,49 Loss of E-cadherin and upregulation of N-cadherin and vimentin expressions are considered to be the major hallmarks of EMT.…”

“…It is well established that OA and its derivatives can block multiple processes of tumor cell invasion (e.g., adhesion, migration and matrix degradation) through the regulation of several signalling pathways (e.g., JNK/p38, MAPK, and PI3K/Akt/mTOR), thereby inhibiting tumor metastasis. 46,47 EMT is a fundamental process that has been implicated in tumor progression. 48,49 Loss of E-cadherin and upregulation of N-cadherin and vimentin expressions are considered to be the major hallmarks of EMT.…”

TFF3 promotes clonogenic survival of colorectal cancer cells through upregulation of EP4 via activation of STAT3

“…Clonogenic assays were performed as previously described ( 19 ). The cells were cultured for about 15 days until visible clones emerged.…”

Construction of a multiple-class classifier based on mRNAs and lncRNA FAM66A and PSORS1C3 for predicting distant metastasis in lung adenocarcinoma

“…Long non-coding RNA (lncRNA) gene expression plays an important role in the early stages of pre-invasive LUAD ( 11 ). Some studies screening and evaluation of hub genes for predicting distant metastasis in lung adenocarcinoma, others suggested that some lncRNAs involved in specific signaling pathways could regulate the development of LUAD ( 12 , 13 ). In addition, lncRNAs have been found to reinforce migration and the invasion of LUAD cells by directly binding to the related factors or increasing oxidative stress ( 14 , 15 ).…”