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Research Paper|Volume 14, Issue 22|pp 9149—9166

LINC00629, a KLF10-responsive lncRNA, promotes the anticancer effects of apigenin by decreasing Mcl1 stability in oral squamous cell carcinoma

Chun Shi1, Changhong Ma3, Chunmei Ren1, Na Li4, Xiaotong Liu1, Yahan Zhang2, Yulong Wang2, Xiaodong Li2, Peng Lv1, Chuanchun Han2, Xiaojie Li1
  • 1College of Stomatology and The Second Hospital, Dalian Medical University, Dalian 116027, China
  • 2Institute of Cancer Stem Cell, Dalian Medical University, Dalian 116027, China
  • 3Department of Otorhinolaryngology, The First Affiliated Hospital, Dalian Medical University, Dalian 116027, China
  • 4National-Local Joint Engineering Research Center for Drug-Research and Development (R&D) of Neurodegenerative Diseases, Dalian Medical University, Dalian 116044, China
* Equal contribution
Received: July 13, 2022Accepted: November 14, 2022Published: November 28, 2022

Copyright: © 2022 Shi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Apigenin, a naturally occurring flavonoid, is known to exhibit antitumor activity in many cancers. However, the regulatory mechanism of apigenin and the long noncoding RNAs (lncRNAs) altered upon apigenin treatment in oral squamous cell carcinoma (OSCC) remain unclear. In this study, we found that LINC00629 was significantly upregulated in response to apigenin treatment. Upregulated LINC00629 enhanced the growth-suppressive and proapoptotic effects of apigenin on OSCC cells by interacting with Mcl1 and facilitating its degradation. Subsequently, our data indicated that KLF10, an important transcription factor, directly bound to the promoter of LINC00629, facilitating its transcription and contributing to apigenin-induced LINC00629 expression. Collectively, these results suggest that the KLF10-LINC00629-Mcl1 axis plays an important role in the anticancer effects of apigenin.