CircRNA circ_0006677 Inhibits the Progression and Glycolysis in Non–Small-Cell Lung Cancer by Sponging miR-578 and Regulating SOCS2 Expression

Abstract

Objective: Circular RNAs (circRNAs) have been demonstrated in playing an important role in the physiological and pathological processes (such as cancer). This paper aims to clarify the role of Circ_0006677 in non–small-cell lung cancer (NSCLC) progression.Methods: Using clinical data and in vitro cell line models, we revealed the tumor-suppressive role of circ_0006677 in lung cancer. Using the online bioinformatics tool, we predicted the target of circ_0006677 and further validated its regulatory mechanisms responsible for its tumor suppressor function in NSCLC.Results: Circ_0006677 expression was reduced in NSCLC tissues of patients and lung cancer cells in comparison to adjacent normal tissues. Lower expression of circ_0006677 was significantly associated with poorer patient survival. Overexpression of circ_0006677 significantly inhibited the ability of NSCLC cell proliferation, migration, invasion, and glycolysis. Mechanically, circ_0006677 could inhibit NSCLC progression and glycolysis by regulating the expression of the signal transducer inhibitor SOSC2 through sponging microRNA-578 (miR-578).Conclusion: Circ_0006677 prevents the progression of NSCLC via modulating the miR-578/SOSC2 axis.

circ_0008797 attenuates non‐small cell lung cancer proliferation, metastasis, and aerobic glycolysis by sponging miR‐301a‐3p/SOCS2

“…Simultaneously, SOCS2 expression can be positively regulated by circ_0006677. circ_0006677 can reduce NSCLC cells growth by suppressing glucose consumption and lactate production via sponging miR‐578 8 . Consistence with the above previous data, the present work verified that SOCS2 was lowly expressed in NSCLC.…”

“…More importantly, through Starbase, circ_0008797 was discovered to have mutual binding site to miR‐301a‐3p, and miR‐301a‐3p possessed mutual binding site for SOCS2. Highly expressed miR‐301a‐3p and lowly expressed SOCS2 has been found in lung cancer cells according to previous studies, resulting in the malignant progression of lung cancer 8,15 . Thus, this research speculated that circ_0008797 might mediate NSCLC progression via targeting miR‐301a‐3p/SOCS2.…”

“…Currently, multiple circRNAs function in NSCLC has been identified. Overall, these circRNAs regulate NSCLC progression by regulating important biological processes, including proliferation, migration, apoptosis, invasion, cell cycle, glucolysis, drug resistance and so forth 5–7 One of the main functions of circRNAs to mediate multiple malignant tumors progression, including NSCLC, is via acting as sponges of microRNAs (miRNAs) 4,8 . For example, circ_0020123 was researched to promote invasion and inhibit apoptosis of NSCLC cells by sponging miR‐384 9 .…”

“…Overall, these circRNAs regulate NSCLC progression by regulating important biological processes, including proliferation, migration, apoptosis, invasion, cell cycle, glucolysis, drug resistance and so forth [5][6][7] One of the main functions of circRNAs to mediate multiple malignant tumors progression, including NSCLC, is via acting as sponges of microRNAs (miRNAs). 4,8 For example, circ_0020123 was researched to promote invasion and inhibit apoptosis of NSCLC cells by sponging miR-384. 9 circ_0004015 and circ-CPA4 was conductive to NSCLC progression, because it exacerbated NSCLC cells proliferation, stemness, immune evasion, and drug resistance by sponging miR-1183 and let-7 miRNA.…”

Elevated Stratifin promotes cisplatin-based chemotherapy failure and poor prognosis in non-small cell lung cancer

“…Briefly, a retroviral vector containing human SFN cDNA with an N-terminal FLAG-tag, vector for constitutive expression of VSV-G glycoprotein (pHCMV-G), and pCMV-dR8.9 were co-transfected into 293T cells, and the viral supernatants were collected to infect A549 cells. 29 Monoclonal cells were then selected, cloned, and screened for SFN expression.…”