C1QTNF6 regulated by miR‐29a-3p promotes proliferation and migration in stage I lung adenocarcinoma

Abstract

Objective C1QTNF6 has been implicated as an essential component in multiple cellular and molecular preliminary event, including inflammation, glucose metabolism, endothelial cell modulation and carcinogenesis. However, the biological process and potential mechanism of C1QTNF6 in lung adenocarcinoma (LUAD) are indefinite and remain to be elucidated. Therefore, we investigated the interaction among the traits of C1QTNF6 and LUAD pathologic process. Methods RT-qPCR and western blot were conducted to determine the expression levels of C1QTNF6. RNA interference and overexpression of C1QTNF6 were constructed to identify the biological function of C1QTNF6 in cellular proliferative, migratory and invasive potentials in vitro. Dual-luciferase reporter assay was applied to identify the possible interaction between C1QTNF6 and miR‐29a-3p. Moreover, RNA sequencing analysis of C1QTNF6 knockdown was performed to identify the potential regulatory pathways. Results C1QTNF6 was upregulated in stage I LUAD tissues compared with adjacent non-cancerous tissues. Concurrently, C1QTNF6 knockdown could remarkably inhibit cell proliferation, migratory and invasive abilities, while overexpression of C1QTNF6 presented opposite results. Additionally, miR‐29a-3p may serve as an upstream regulator of C1QTNF6 and reduce the expression of C1QTNF6. Subsequent experiments showed that miR‐29a-3p could decrease the cell mobility and proliferation positive cell rates, as well as reduce the migratory and invasive possibilities in LUAD cells via downregulating C1QTNF6. Moreover, RNA sequencing analysis demonstrated that the cytokine-cytokine receptor interaction pathway may participate in the process of C1QTNF6 regulating tumor progression. Conclusion Our study first demonstrated that downregulation of C1QTNF6 could inhibit tumorigenesis and progression in LUAD cells negatively regulated by miR‐29a-3p. These consequences could reinforce our awareness and understanding of the underlying mechanism and provide a promising therapeutic target for LUAD.

Liquid Biopsy in non-small cell lung cancer: exosomes as a tool for the study of biomarkers.

“…However, miR-29a-3p expression has been observed in lung adenocarcinoma cells. Studies have found that overexpression of miR-29a-3p is associated with cell proliferation, migration and invasion in LUAD cells [300]. These findings may be related to the observed overexpression of this biomarker in our LUAD-derived exosome samples.…”

Novel genome-wide DNA methylation profiling reveals distinct epigenetic landscape, prognostic model and cellular composition of early-stage lung adenocarcinoma

“…E2F7 and ANLN, were both involved in the cell cycle process and associated with cell proliferation in malignancy lung cancer [ 67 – 70 ]. C1QTNF6 had been found to be upregulated in stage I lung cancer tissue and regulated by MIR-29 A-3P to promote proliferation [ 71 ]. What’s more, inhibition of C1QTNF6 could attenuated cell migration, invasion and promoted apoptosis in non-small cell lung cancer [ 72 ].…”

Text mining and data analysis identifies potential drugs and pathways for polycystic ovary syndrome treatment

“…Studies related to the cytokine–cytokine receptor interaction pathway have been conducted in many other diseases, as well as pathways that are potentially involved in PCOS. For instance, a study by Lin et al proposed that the miR-29a-3p/C1QTNF6 regulatory axis may promote proliferation and migration in stage I lung adenocarcinoma through the cytokine–cytokine receptor interaction pathway [20] . Another study revealed that SRMS modulates the cytokine–cytokine receptor interaction pathway to regulate colorectal cancer (CRC) progression in colorectal carcinoma patients [21] .…”