2. Academic Validation
  3. OPA1 supports mitochondrial dynamics and immune evasion to CD8+ T cell in lung adenocarcinoma

OPA1 supports mitochondrial dynamics and immune evasion to CD8+ T cell in lung adenocarcinoma

  • PeerJ. 2022 Dec 21;10:e14543. doi: 10.7717/peerj.14543.
Ying Wang # 1,  Yadong Li # 2,  Xuanwei Jiang 3,  Yayun Gu 3,  Hui Zheng 1,  Xiaoxuan Wang 4,  Haotian Zhang 5,  Jixiang Wu 6 7,  Yang Cheng 1
Affiliations

Affiliations

  • 1 Center for Health Management, Jiangsu Province Geriatric Hospital, Nanjing, China.
  • 2 Department of Thoracic Surgery, The Second Clinical Medical College of Nanjing Medical University, Nanjing, China.
  • 3 State Key Laboratory of Reproductive Medicine, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China.
  • 4 State Key Laboratory of Translational Medicine and Innovative Drug Development, Jiangsu Simcere Diagnostics Co., Ltd., Nanjing, China.
  • 5 The First Clinical Medical College of Nanjing Medical University, Nanjing, China.
  • 6 Department of Thoracic and Cardiovascular Surgery, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, China.
  • 7 Department of Thoracic and Cardiovascular Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng, China.
  • # Contributed equally.
PMID: 36573240 DOI: 10.7717/peerj.14543
Abstract

Background: Mitochondrial fusion and fission were identified to play key roles during multiple biology process. Thus, we aim to investigate the roles of OPA1 in mitochondria fusion and immune evasion of non-small cell lung Cancer cells.

Methods: The transcriptional activation of genes related to mitochondrial dynamics was determined by using multi-omics data in lung adenocarcinoma (LUAD). We elucidated the molecular mechanism and roles of OPA1 promoting lung Cancer through single-cell Sequencing and molecular biological experiments.

Results: Here, we found that copy number amplification of OPA1 and MFN1 were co-occurring and synergistically activated in tumor epithelial cells in lung Cancer tissues. Both of OPA1 and MFN1 were highly expressed in LUAD tumor tissues and OPA1 high expression was associated with poor prognosis. In terms of mechanism, the damaged mitochondria activated the apoptotic signaling pathways, inducing cell cycle arrest and cell Apoptosis. More interestingly, OPA1 deficiency damaged mitochondrial dynamics and further blocked the respiratory function to increase the sensitivity of tumor epithelial to CD8+ T cells in non-small cell lung Cancer.

Conclusions: Our study demonstrated the high co-occurrence of copy number amplification and co-expression of OPA1 and MFN1 in LUAD tissue, and further revealed the contribution of OPA1 in maintaining the mitochondria respiratory function and the ability of immune evasion to CD8+ T cells of LUAD.

Keywords

CD8+ T cell; Immune evasion; Lung adenocarcinoma; Mitochondrial fusion; OPA1.

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