2. Academic Validation
  3. RPL11 promotes non-small cell lung cancer cell proliferation by regulating endoplasmic reticulum stress and cell autophagy

RPL11 promotes non-small cell lung cancer cell proliferation by regulating endoplasmic reticulum stress and cell autophagy

  • BMC Mol Cell Biol. 2023 Mar 3;24(1):7. doi: 10.1186/s12860-023-00469-2.
Jie Chen # 1 2,  Changda Lei # 3,  Huahua Zhang # 1 2,  Xiaoyong Huang 1 2,  Yang Yang 1 2,  Junli Liu 1 2,  Yuna Jia 1 2,  Haiyan Shi 1 2,  Yunqing Zhang 4,  Jing Zhang 5 6,  Juan Du 7 8
Affiliations

Affiliations

  • 1 Medical Research and Experimental Center, Medical College, Yan'an University, 716000, Yan'an, People's Republic of China.
  • 2 Yan'an Key Laboratory of Chronic Disease Prevention and Research, 716000, Yan'an, Shaanxi Province, China.
  • 3 Department of Gastroenterology, Ninth Hospital of Xi 'an, 710054, Xi'an, Shaanxi Province, China.
  • 4 Laboratory of Obstetrics and Gynecology, Affiliated Hospital of Yan'an University, 716000, Yan'an, Shaanxi Province, China. [email protected].
  • 5 Medical Research and Experimental Center, Medical College, Yan'an University, 716000, Yan'an, People's Republic of China. [email protected].
  • 6 Yan'an Key Laboratory of Chronic Disease Prevention and Research, 716000, Yan'an, Shaanxi Province, China. [email protected].
  • 7 Medical Research and Experimental Center, Medical College, Yan'an University, 716000, Yan'an, People's Republic of China. [email protected].
  • 8 Yan'an Key Laboratory of Chronic Disease Prevention and Research, 716000, Yan'an, Shaanxi Province, China. [email protected].
  • # Contributed equally.
PMID: 36869281 DOI: 10.1186/s12860-023-00469-2
Abstract

Background: Abnormal biogenesis and ribosome free function of ribosomal proteins (RPs) is important for tumorgenesis and development. Ribosomal protein L11 (RPL11) is a component of ribosomal 60 S large subunit with different roles in different cancers. Here, we aimed to unravel the role of RPL11 in non-small cell lung Cancer (NSCLC), especially those affecting cell proliferation.

Methods: RPL11 expression in NCI-H1650, NCI-H1299, A549 and HCC827 and normal lung bronchial epithelial cells HBE was detected using western blotting. The function of RPL11 in NSCLC cells were determined by investigating cell viablity, colony formation and cell migration. Mechanism expoloration of RPL11 effect on NSCLC cells proliferation was explored using flow cytometry, and the effect on Autophagy was investigated by the additon of Autophagy Inhibitor chloroquine (CQ) and endoplasmic reticulum stress (ERS) inhibitor tauroursodeoxycholic acid (TUDCA).

Results: RPL11 was highly expressed in NSCLC cells. Extopic expression of RPL11 promoted NCI-H1299 and A549 cells proliferation, and migration, and promoted the transition from the G1 phase to the S phase of the cell cycle. Small RNA interference of RPL11 (siRNA) suppressed NCI-H1299 and A549 cells proliferation and migration and arrested the cell cycle in G0/G1 phase. Moreover, RPL11 promoted NSCLC cell proliferation by modulating Autophagy and ERS. Expression levels of Autophagy and ERS markers were induced by RPL11 overexpression and inhibited by siRPL11. CQ partially suppressed RPL11-induced A549 and NCI-H1299 proliferation: CQ addition reduced RPL11-induced cells viability and clone numbers and reversed the cell cycle process. ERS inhibitor (TUDCA) partially reversed RPL11-induced Autophagy.

Conclusion: Taken together, RPL11 has a tumor-promoting role in NSCLC. It promotes the cell proliferation of NSCLC cells by regulating ERS and Autophagy.

Keywords

Autophagy; Endoplasmic reticulum stress; Non-small cell lung cancer (NSCLC); RPL11.

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