ArticleWorld journal of surgical oncology2025
UBC9 overexpression promotes proliferation and metastasis in gastric cancer via ATF2.
Article in World journal of surgical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Mechanistic investigation of TRIB3-mediated growth, metastasis and ferroptosis in renal cell carcinoma.Human cell · 2026Article
- Long non-coding RNA SOCS2-AS1 inhibits gastric cancer progression via the miR-324-3p/GRIK3 axis: a mechanistic study.World journal of surgical oncology · 2026Article
- UBC9-mediated SUMOylation of CORO1C drives lung adenocarcinoma progression via Arp2/3-dependent cytoskeletal remodeling.Cell death & disease · 2026Article
- UBC9-mediated regulation of K144 ubiquitination of Lamin A and its implications for hepatocellular carcinoma.Journal of translational medicine · 2026Article
- Glycosylation-Related Gene Signature Identifies MFNG as a Key Driver of Proliferation and Metastasis in Colorectal Cancer.OncoTargets and therapy · 2026Article
- Ubiquitin-conjugating Enzymes in Cancer.International journal of biological sciences · 2026Review
- UBC9 mediates mitophagy to attenuate oxidative stress by regulating SUMOylation of PINK1 in the Parkinson's disease progression.Cell biology and toxicology · 2025Article
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Authors and funding
19 authors.
Funding
Abstract
Gastric cancer remains a leading cause of cancer-related mortality worldwide, characterized by poor prognosis due to its aggressive nature and high metastatic potential. While the E2-conjugating enzyme UBE2I (UBC9), essential for SUMOylation, has been implicated in various cancers, its precise role in gastric cancer remains poorly understood. In the study, we demonstrate significant UBC9 overexpression in gastric cancer tissues, which correlates with poor clinical outcomes. Functional analyses revealed that UBC9 knockdown significantly suppressed gastric cancer cell proliferation, migration, and invasion in vitro and in vivo, whereas UBC9 overexpression enhanced these malignant phenotypes. Through integrated transcriptomic and proteomic analyses, we identified ATF2 (Activating Transcription Factor 2) as a crucial downstream effector of UBC9-mediated oncogenic signaling. The mechanistic relationship between these factors was confirmed as ATF2 knockdown substantially attenuated the oncogenic effects of UBC9 overexpression. This newly identified UBC9-ATF2 regulatory axis promotes gastric cancer progression by enhancing cellular proliferation and metastatic potential. Our findings establish UBC9 and ATF2 as promising prognostic biomarkers and potential therapeutic targets, suggesting that intervention in the UBC9-ATF2 axis may provide novel therapeutic strategies for inhibiting gastric cancer progression and improving patient outcomes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.