FAM83A and FAM83A‑AS1 both play oncogenic roles in lung adenocarcinoma

Abstract

Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Nevertheless, the detailed molecular mechanisms of the progression of LUAD remain largely unknown. The present bioinformatics analysis reported that FAM83A and FAM83A-AS1 were upregulated in LUAD tissues and associated with prognosis in patients with LUAD. The purpose of the current study was to investigate the role of FAM83A and its antisense long non-coding (lnc)RNA FAM83A-AS1 in LUAD. Gene Expression Profiling Interactive Analysis was used to screen for potential oncogenes in LUAD and to analyze the clinical significance of FAM83A and FAM83A-AS1. Small interfering RNAs were constructed and transfected into LUAD cells to knock down the expression of FAM83A and FAM83A-AS1. EdU, Cell Counting Kit-8, Transwell and Matrigel assays were performed to detect the proliferation, migration and invasion of LUAD cells. The interaction between FAM83A-AS1, microRNA (miR)-495-3p and FAM83A was explored using a luciferase reporter assay. FAM83A and FAM83A-AS1 were both overexpressed in LUAD tissues compared with adjacent normal tissues. High expression of FAM83A and FAM83A-AS1 predicted worse survival and more advanced clinical stage. Knockdown of FAM83A or FAM83A-AS1 could inhibit the proliferation, migration and invasion of LUAD cells. Moreover, lncRNA FAM83A-AS1 regulated the expression of FAM83A by functioning as competing endogenous RNA for miR-495-3p. These results implicated that FAM83A and FAM83A-AS1 both played oncogenic roles in LUAD and FAM83A-AS1 could regulate the expression of FAM83A by sponging miR-495-3p. The study revealed a novel regulatory mechanism of tumor development in LUAD and FAM83A and FAM83A-AS1 may be novel biomarkers and therapeutic targets for LUAD.

LncRNA FAM83A-AS1 facilitates tumor proliferation and the migration via the HIF-1α/ glycolysis axis in lung adenocarcinoma

“…Many studies have reported that lncRNA, FAM83A-AS1 has potent tumor-promoting activity in oesophageal squamous cell carcinoma (ESCC), lung cancer, and liver carcinoma [25][26][27]. For instance, Xiao G et al [28] discovered that FAM83A-AS1 could promote LUAD cell migration and invasion, consistent with our results.…”

YTHDF2 Inhibits the Migration and Invasion of Lung Adenocarcinoma by Negatively Regulating the FAM83D-TGFβ1-SMAD2/3 Pathway

“…Recent studies have revealed that most of these members are closely related to the occurrence and development of various types of cancer. As reported by Wang G et al, FAM83A has been confirmed to be highly expressed in lung adenocarcinoma and is associated with a poor prognosis (24). FAM83B inhibits cisplatin resistance in ovarian cancer by inhibiting the Wnt pathway (25), and high FAM83F expression plays a pro-oncogenic role in papillary thyroid cancer (26).…”

FAM83A antisense RNA 1 (FAM83A-AS1) silencing impairs cell proliferation and induces autophagy via MET-AMPKɑ signaling in lung adenocarcinoma

“…FAM83A-AS1 plays oncogenic roles in esophageal, liver, and lung cancers [ 18–21 , 23–25 ]. We found that knockdown of FAM83A-AS1 decreased the cell proliferation, colony formation, invasion, and migration in H1299 and H838 lung cancer cells, which were consistent with others [ 18–21 , 40 ].…”

“…It was reported FAM83A-AS1 expression is higher in esophageal cancer and can promote cancer progression via binding of miR-495-3p [ 18 ]; whereas knockdown of FAM83A-AS1 impaired cell growth and induced cell apoptosis through binding of NOP58 in liver cancer [ 19 ]. FAM83A-AS1 was suggested to affect lung cancer cell invasion and migration through miR-150-5p/MMP14 signaling [ 20 ] or miR-495-3p [ 23 ] and may promote lung cancer progression through increasing FAM83A expression [ 21 , 24 ] or glycolysis via regulating HIF-1α degradation [ 26 ]. However, the detailed mechanism of FAM83A-AS1 in lung cancer remains uncertain.…”