2. Academic Validation
  3. Overexpression of LINC00551 promotes autophagy-dependent ferroptosis of lung adenocarcinoma via upregulating DDIT4 by sponging miR-4328

Overexpression of LINC00551 promotes autophagy-dependent ferroptosis of lung adenocarcinoma via upregulating DDIT4 by sponging miR-4328

  • PeerJ. 2022 Oct 12:10:e14180. doi: 10.7717/peerj.14180.
Xiong Peng 1 2,  Rui Yang 3,  Weilin Peng 1 2,  Zhenyu Zhao 1 2,  Guangxu Tu 1 2,  Boxue He 1 2,  Qidong Cai 1 2,  Shuai Shi 1 2,  Wei Yin 1 2,  Fenglei Yu 1 2,  Yongguang Tao 1 4 5,  Xiang Wang 1 2
Affiliations

Affiliations

  • 1 Department of Thoracic Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
  • 2 Hunan Key Laboratory of Early Diagnosis and Precise Treatment of Lung Cancer, the Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
  • 3 Department of Pathology, School of Basic Medicine and Xiangya Hospital, Central South University, Changsha, Hunan, China.
  • 4 NHC Key Laboratory of Carcinogenesis (Central South University), Cancer Research Institute and School of Basic Medicine, Central South University, Changsha, Hunan, China.
  • 5 Department of Pathology, Xiangya Hospital, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Central South University, Changsha, Hunan, China.
PMID: 36570007 DOI: 10.7717/peerj.14180
Abstract

According to mounting evidence, long noncoding RNAs (lncRNAs) play a vital role in regulated cell death (RCD). A potential strategy for Cancer therapy involves triggering Ferroptosis, a novel form of RCD. Although it is thought to be an autophagy-dependent process, it is still unclear how the two processes interact. This study characterized a long intergenic noncoding RNA, LINC00551, expressed at a low level in lung adenocarcinoma (LUAD) and some Other cancers. Overexpression of LINC00551 suppresses cell viability while promoting Autophagy and RSL-3-induced Ferroptosis in LUAD cells. LINC00551 acts as a competing endogenous RNA (ceRNA) and binds with miR-4328 which up-regulates the target DNA damage-inducible transcript 4 (DDIT4). DDIT4 inhibits the activity of mTOR, promotes LUAD Autophagy, and then promotes the Ferroptosis of LUAD cells in an autophagy-dependent manner. This study provided an insight into the molecular mechanism regulating Ferroptosis and highlighted LINC00551 as a potential therapeutic target for LUAD.

Keywords

Autophagy; DDIT4; Ferroptosis; LINC00551; Lung adenocarcinoma.

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