LINC00313 suppresses autophagy and promotes stemness of nasopharyngeal carcinoma cells through PTBP1/STIM1 axis

Lina Xu; Sile Liu; Yang Yang; Lu Shu; Yi Sun

doi:10.1016/j.radonc.2024.110310

LINC00313 suppresses autophagy and promotes stemness of nasopharyngeal carcinoma cells through PTBP1/STIM1 axis

Radiother Oncol. 2024 Apr 26:196:110310. doi: 10.1016/j.radonc.2024.110310. Online ahead of print.

Authors

Lina Xu¹, Sile Liu², Yang Yang¹, Lu Shu³, Yi Sun⁴

Affiliations

¹ Department of Pathology, The Second Xiangya Hospital of Central South University, Changsha 410011, Hunan Province, PR China.
² Department of Laboratory Medicine, Hunan Provincial People's Hospital, Changsha 410005, Hunan Province, PR China.
³ Department of Thoracic Surgery, The Second Xiangya Hospital of Central South University, Changsha 410011, Hunan Province, PR China.
⁴ Department of Pathology, The Second Xiangya Hospital of Central South University, Changsha 410011, Hunan Province, PR China. Electronic address: yyssuunn987@163.com.

PMID: 38677328
DOI: 10.1016/j.radonc.2024.110310

Abstract

Background: Nasopharyngeal carcinoma (NPC) is a kind of malignant head and neck tumor with high mortality. lncRNAs are valuable diagnostic biomarkers and therapeutic targets for various tumors. This study investigated the effects and mechanism of LINC00313 in nasopharyngeal carcinoma.

Methods: Cell Counting Kit-8 (CCK-8) and immunohistochemistry were used for assessing cell proliferation. The levels of autophagy-related proteins, and stem cell markers were detected. Immunofluorescence assay was used for LC3 detection. Methylated RNA Immunoprecipitation (meRIP) of LINC00313 in NPC cells was assessed. The localization of LINC00313 was verified by luorescence in situ hybridization (FIHS). The interaction between LINC00313 and the downstream targets were analyzed and confirmed by immunoprecipitation (RIP). Besides, the tumorigenesis roles of LINC00313 were confirmed in tumor growth mice model.

Results: LINC00313 was increased in NPC tissues and cells. LINC00313 knockdown enhanced autophagy, and decreased stemness and cell viability of NPC cells through regulating STIM1. METTL3/IGF2BP1-mediated m6A modification promoted the stabilization and up-regulation of LINC00313. LINC00313 activated AKT/mTOR pathway in NPC cells through PTBP1/STIM1 axis. Moreover, LINC00313 promoted tumor growth and metastasis in xenograft model.

Conclusion: Upregulation of LINC00313 suppressed autophagy and promoted stemness of NPC cells through PTBP1/STIM1 axis.

Keywords: Autophagy; LINC00313; Nasopharyngeal carcinoma; STIM1; Stemness.