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Published on: October 27, 2020
Troponin C-1 Activated by E2F1 Accelerates Gastric Cancer Progression via Regulating TGF-β/Smad Signaling
Can Fang1, Xinxin Zhang1, Chengyan Li2
1Department of Gastroenterology, Yantai Affiliated Hospital of Binzhou Medical University, 717 Jinbu Street, Muping District, Yantai, 264100, Shandong, People's Republic of China.
Background:
Troponin C-1 (TNNC1) has been previously characterized as an oncogenic gene.
Aims:
This study aimed to reveal the roles of TNNC1 in gastric cancer and the potential underlying mechanisms.
Methods:
TNNC1 siRNAs and TNNC1 overexpression plasmid were used to alter its expression in AGS, MKN45, and HGC-27 cells. CCK-8 assay, colony formation, EdU assay, flow cytometry, transwell assay, and scratch test were conducted to measure the phenotype changes. In vivo effects of TNNC1 silence were confirmed by using a xenograft mouse model. Bioinformatics analysis was conducted to screen out the transcription factor and downstream signaling of TNNC1.
Results:
TNNC1 was highly expressed in gastric cancer tissues and cell lines, and its expression was associated with poor prognosis. TNNC1 silence suppressed the proliferation, migration, and invasion of AGS and MKN45 cells. However, TNNC1 silence induced apoptosis by mediating the cleavage of caspase-3 and caspase-9. Overexpression of TNNC1 in HGC-27 cells led to the contrary effects. The anti-tumor effects of TNNC1 silence were also confirmed in a xenograft animal model. E2F1 was validated as an upstream transcription factor of TNNC1. Effects of TNNC1 silence on AGS cell migration and invasion were attenuated by E2F1 overexpression. Besides, TGF-β/Smad was a downstream signaling pathway of TNNC1. The anti-tumor impacts of TNNC1 silence were weaken by SB431542 (a specific inhibitor of TGF-β signaling) while accelerated by TGF-β.
Conclusion:
TNNC1 activated by E2F1 functioned as an oncogenic gene through regulating TGF-β/Smad signaling. TNNC1 was suggested as a potential molecular drug target of gastric cancer.
Insights
Troponin C-1 (TNNC1) acts as an oncogene in gastric cancer, promoting proliferation and invasion. Targeting TNNC1, activated by E2F1 and regulating TGF-β/Smad signaling, offers a potential therapeutic strategy.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Troponin C-1 (TNNC1) is recognized as an oncogenic gene.
- Gastric cancer remains a significant global health challenge with a need for novel therapeutic targets.
Purpose of the Study:
- To elucidate the specific roles of TNNC1 in gastric cancer progression.
- To identify the molecular mechanisms and signaling pathways regulated by TNNC1 in gastric cancer.
Main Methods:
- Utilized TNNC1 siRNA and overexpression plasmids in gastric cancer cell lines (AGS, MKN45, HGC-27).
- Assessed cellular phenotypes using CCK-8, colony formation, EdU, flow cytometry, Transwell, and scratch assays.
- Validated findings in a xenograft mouse model and employed bioinformatics for pathway analysis.
Main Results:
- TNNC1 exhibited high expression in gastric cancer tissues and correlated with poor prognosis.
- TNNC1 knockdown inhibited proliferation, migration, and invasion, while inducing apoptosis.
- E2F1 was identified as an upstream regulator, and TGF-β/Smad signaling as a downstream pathway affected by TNNC1.
Conclusions:
- TNNC1, activated by E2F1, promotes gastric cancer via TGF-β/Smad signaling.
- TNNC1 represents a promising molecular target for gastric cancer therapy.
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