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Abstract
The long noncoding RNA called MIR22 host gene (MIR22HG) was previously identified as a tumor suppressor in several cancers. However, the biological function of MIR22HG in breast cancer remains unknown. In this study, we aimed to determine the function and molecular mechanism of MIR22HG in breast cancer progression using transcriptomics and biotechnological techniques. Our results showed that MIR22HG expression was lower in the cancerous tissues than in the paired adjacent normal breast tissues. Additionally, MIR22HG was found to be mainly located in the cytoplasm and acted as a miR-629-5p sponge. Notably, MIR22HG stabilized the expression of large tumor suppressor 2 (LATS2), which promoted the LATS2-dependent phosphorylation of YAP1 and suppressed the expression of its downstream target oncogenes, thereby inhibiting the proliferation and migration of breast cancer cells. Therefore, our findings reveal the MIR22HG-dependent inhibition of breast cancer cell proliferation and migration via the miR-629-5p/LATS2 pathway, providing new insights and identifying novel therapeutic targets for breast cancer treatment.
Highlights
As the most commonly diagnosed cancer worldwide, female breast cancer had an estimated incidence rate of 11.7% in 2020 and was known to greatly influence women’s health [1]
MIR22 host gene (MIR22HG) expression is downregulated in breast cancer tissues To investigate MIR22HG expression in breast cancer tissues, we collected 36 pairs of cancerous tissues and adjacent normal breast tissues for real-time PCR analysis
Our results showed that in most paired tissues (26/36), MIR22HG expression was lower in cancerous tissues than in normal tissues (Fig. 1a)
Summary
As the most commonly diagnosed cancer worldwide, female breast cancer had an estimated incidence rate of 11.7% in 2020 and was known to greatly influence women’s health [1]. Increasing evidences show that long noncoding RNAs (lncRNAs) play important roles in breast cancer progression [2]. Several lncRNAs, such as MALAT1 [4], RAB11B-AS1 [5], TROJAN [6], and HOST2 [7], have been found to facilitate the proliferation and metastasis of breast cancer cells. TROJAN interacts with metastasisrepressing factor ZMYND8, subsequently increasing ZMYND8 degradation via the ubiquitin-proteasome pathway by repelling ZNF592, and enhancing cancer progression [6]. HOST2 was revealed to act as a competitive endogenous RNA via decoying of let-7b, thereby promoting STAT3-mediated cell proliferation and migration in triple-negative breast cancer [7]
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