COX6B2 drives metabolic reprogramming toward oxidative phosphorylation to promote metastasis in pancreatic ductal cancer cells
Open accessAbstract
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer type with poor prognosis due to its high metastatic potential, however, the role of metabolic reprogramming in the metastasis of PDAC cell is not known. Here, we report that COX6B2 drive metastasis but not cancer cell proliferation in PDAC by enhancing oxidative phosphorylation function (OXPHOS). Transcriptome and clinical analyses revealed that cytochrome c oxidase subunit 6B2 (COX6B2) positively associated with metastasis of PDAC cells. Knockdown of COX6B2 in PDAC cells tuned down the assembly of complex IV and downregulated the function of OXPHOS, whereas re-expression of COX6B2 restored the function of OXPHOS and metastatic potential. Mechanistically, COX6B2 upregulated OXPHOS function to active purinergic receptor pathway for the metastasis of PDAC cells. Notably, the metastatic potential in PDAC could be reversely regulated by metformin, a drug was found accelerating the degradation of COX6B2 mRNA in this study. Collectively, our findings indicated that a complex metabolic control mechanism might be involved in achieving the balance of metabolic requirements for both growth and metastasis in PDAC, and regulation of the expression of COX6B2 could potentially encompass one of the targets.
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Pancreatic ductal adenocarcinoma (PDAC) lines were chosen because cancers of the pancreas are characterized by rapid progression, invasiveness, and elevated fermentative metabolism.
“Pancreatic ductal adenocarcinoma (PDAC) lines were chosen for our study because cancers of the pancreas are characterized by rapid progression,9,10 invasiveness,11,12 and elevated fermentative metabolism.13,14,15,16”
From Dynamic IL-6R/STAT3 signaling leads to heterogeneity of metabolic phenotype in pancreatic ductal adenocarcinoma cells (2024) · cites this paper as [12]
The Introduction describes PDAC as highly aggressive, with patients often dying within months, and attributes its aggressiveness partly to high metastatic potential. It reports both Warburg and anti-Warburg metabolism in PDAC, however, so it does not support characterizing pancreatic cancers generally by elevated fermentative metabolism. (LLM, conf=0.88)
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- Authors
- Nie, K., Li, J., He, X., Wang, Y., Zhao, Q., Du, M., Sun, H., Wang, J., Lyu, J., Fang, H., & Jin, L.
- Affiliations
- Wenzhou Medical University (CN)
- Hangzhou Medical College (CN)
- First Affiliated Hospital of Wenzhou Medical University (CN)
- Corresponding author
- Lyu, Jianxin
- Fang, Hezhi
- Jin, Liqin
- ORCID
- Venue
- Oncogenesis
- Published
- 2020-05-15
- Volume
- 9
- Issue
- 5
- Pages
- 51-51
- ISSN
- 2157-9024 (ISSN-L)
- PMC
- PMC7229118
- OpenAlex
- W3025982311
- Cited by
- 64
- References
- 41
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 7 · 2023: 13 · 2022: 10 · 2021: 10 · 2020: 6
- FWCI
- 3.51
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Oncogenesis (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- the Key Discipline of Zhejiang Province in Medical Technology
- Natural Science Foundation of Zhejiang Province (LY20H160012)
- National Natural Science Foundation of China (81830071, 31670784)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- pancreatic ductal adenocarcinoma, metastasis, metabolic reprogramming, oxidative phosphorylation, metformin, mRNA degradation, tumor cell proliferation
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