CircPRKCA Promotes NSCLC Progression via miR-200b-3p/FRMD6/SNAI2 Axis

Sep 22, 2026

Circular RNAs (circRNAs) are linked with tumor progression, yet the mechanism of circPRKCA in non-small cell lung cancer (NSCLC) remains unclear. circPRKCA is highly expressed in NSCLC tissues and cells, and its knockdown reduces malignant behaviors. RNA sequencing shows FRMD6 and SNAI2 mRNAs correlate positively with circPRKCA, indicating regulatory involvement. Mechanistically, circPRKCA sponges miR-200b-3p, preventing miR-200b-3p-mediated degradation of FRMD6 and SNAI2 mRNAs. This loss of degradation counteracts miR-200b-3p tumor-suppressive effects, thereby accelerating NSCLC progression through a circPRKCA/miR-200b-3p axis.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages17

Reading Time43 min

AccessFree to download

Abstract

1. Introduction

2. Results

2.1. Identification and Characterization of circPRKCA in Lung Cancer

2.2. CircPRKCA Promotes Malignant Phenotypes in NSCLC Cells

Article CircPRKCA Promotes NSCLC Progression via miR-200b-3p/FRMD6/SNAI2 Axis He Zhong 1,†, Ning Wang 1,†, Hui Zhang 1, Min Chen 1, Xin Liao 2,* and Chao Huang 1, * Academic Editor: Naoyuki Kataoka Received: 11 February 2026 Revised: 9 April 2026 Accepted: 22 April 2026 Published: 25 April 2026 Copyright: © 2026 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license. 1 Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China 2 Department of General Practice, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China * Correspondence: [liaoxin@tjh.tjmu.edu.cn](liaoxin@tjh.tjmu.edu.cn) (X.L.); [huangchaowhuh@hust.edu.cn](huangchaowhuh@hust.edu.cn) (C.H.); Tel.: +86-027-83663392 (X.L.); +86-027-85726337 (C.H.)† These authors contributed equally to this work. Abstract Circular RNAs (circRNAs) have been reported to be closely associated with tumor progression in multiple malignancies. However, the specific mechanism by which circPRKCA influences tumor progression has not been fully elucidated. CircPRKCA is highly expressed in non-small cell lung cancer (NSCLC) tissues and cells. Knockdown of circPRKCA inhibits the malignant behaviors of NSCLC cells. RNA sequencing results revealed that FRMD6 and SNAI2 mRNAs are positively correlated with circPRKCA. Subsequently, we proved that circPRKCA acts as a molecular sponge for miR-200b-3p. Additionally, miR-200b-3p binds to the 3′ untranslated regions (3′UTRs) of FRMD6 and SNAI2 mRNAs to promote their degradation. Overexpression of circPRKCA thereby suppresses this degradation process and coun-teracts the tumor-suppressive effects induced by miR-200b-3p. CircPRKCA functions as the sponge of miR-200b-3p, suppressing the SNAI2 /FRMD6 mRNA degradation driven by miR-200b-3p and accelerating NSCLC progression. Keywords: circPRKCA; non-small cell lung cancer; miR-200b-3p 1. Introduction Circular RNAs (circRNAs) represent a unique class of covalently closed endogenous transcripts that function predominantly as molecular sponges for microRNAs (miRNAs), thereby modulating the expression of downstream target genes [1–3] . Among these, hsa_circ_ 0007580 (termed circPRKCA), derived from the PRKCA gene, has emerged asa critical regulator in non-small cell lung cancer (NSCLC) [4] . While a recent study has underscored the clinical significance of circPRKCA in promoting NSCLC progression, the intricate molecular networks and alternative signaling axes through which it exerts its oncogenic effects remain to be fully mapped. Understanding these unresolved mechanisms is crucial for identifying precise therapeutic targets in circPRKCA-driven malignancies. The Hippo signaling pathway, a highly conserved evolutionary cascade, serves as a fundamental governor of cell proliferation and apoptosis. Dysregulation of this pathway, characterized by the aberrant activation of its key downstream effectors, YAP and TAZ, is frequently observed in NSCLC and correlates with poor prognosis [5–8] . Emerging evidence suggests that circRNAs can act as upstream modulators of the Hippo kinase core, either by sequestering pathway-specific miRNAs or through direct protein interactions [9–11] . However, whether circPRKCA engages the Hippo signaling axis to drive the malignant phenotype of NSCLC cells remains an intriguing and unexplored question. In this study, through high-throughput transcriptome sequencing of NSCLC patient tissues, we identified circPRKCA as a significantly upregulated circular RNA. Clinical correlation analysis and functional assays revealed that circPRKCA acts as a molecular sponge to sequester miR-200b-3p, thereby relieving the inhibitory effect on SNAI2 and FRMD6 expression. This molecular decoy mechanism leads to the const

FAQs

What role does circPRKCA play in NSCLC progression?

circPRKCA is highly expressed in NSCLC and its knockdown inhibits malignant behaviors, indicating it promotes NSCLC progression.

How does circPRKCA regulate miR-200b-3p activity?

circPRKCA functions as a molecular sponge for miR-200b-3p, sequestering it and thereby blocking miR-200b-3p’s downstream effects.

Which downstream targets are affected by the circPRKCA/miR-200b-3p axis?

miR-200b-3p binds the 3′UTRs of FRMD6 and SNAI2 mRNAs to promote their degradation, while circPRKCA counteracts this degradation process and suppresses miR-200b-3p tumor-suppressive effects.

Sep 22, 2026

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