ArticleCancer cell international2020
Suppression of CCT3 inhibits the proliferation and migration in breast cancer cells.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Chaperonin in health and disease.Molecular biomedicine · 2026Review
- Multimodal AI-Driven Identification of Dehydrocostus Lactone as a Potent Renal Fibrosis Attenuator Targeting IQGAP1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CCT7 predicts poor prognosis and correlates with immune infiltration in colonic adenocarcinoma.Journal of molecular histology · 2026Article
- Dual Biological Effects and Mechanisms of Gut Microbiota in Breast Cancer: A Review.Current pharmaceutical biotechnology · 2026Review
- TRIM38 Suppresses the Progression of Colorectal Cancer via Enhancing CCT6A Ubiquitination to Inhibit the MYC Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Prognostic Significance ofIranian journal of biotechnology · 2025Article
- Advances in the study of CCT3 in malignant tumors: A review.Medicine · 2025Review
- Revisiting the chaperonin T-complex protein-1 ring complex in human health and disease: A proteostasis modulator and beyond.Clinical and translational medicine · 2024Review
- A potential tumor marker: Chaperonin containing TCP‑1 controls the development of malignant tumors (Review).International journal of oncology · 2023Review
- Integrated analyzes identify CCT3 as a modulator to shape immunosuppressive tumor microenvironment in lung adenocarcinoma.BMC cancer · 2023Article
- Superenhancer activation of KLHDC8A drives glioma ciliation and hedgehog signaling.The Journal of clinical investigation · 2023Article
- Upregulation of CCT3 predicts poor prognosis and promotes cell proliferation via inhibition of ferroptosis and activation of AKT signaling in lung adenocarcinoma.BMC molecular and cell biology · 2022Article
- Article
- Insights into the roles and driving forces of CCT3 in human tumors.Frontiers in pharmacology · 2022Article
- Current understanding on the role of CCT3 in cancer research.Frontiers in oncology · 2022Review
- The TRiCky Business of Protein Folding in Health and Disease.Frontiers in cell and developmental biology · 2022Review
- Article
- Upregulation of CCT3 promotes cervical cancer progression through FN1.Molecular medicine reports · 2021Article
- Identification of CCT3 as a prognostic factor and correlates with cell survival and invasion of head and neck squamous cell carcinoma.Bioscience reports · 2021Article
- Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCCT3 is a subunit of chaperonin-containing TCP-1 (CCT), which folds many proteins involved in cancer development and plays an important role in many cancers. However, the role of CCT3 in breast cancer is still unclear.
methodsCCT3 expression was knocked down by transfecting breast cancer cells with lentiviral shRNA. The proliferation of breast cancer cells (HCC1937 and MDA-MB-231) was detected by Celigo image cytometry and MTT assay, the migration of the cells was measured by Transwell analysis, cell cycle distribution and apoptosis was detected by flow cytometry, and changes in signal transduction proteins were detected by western blot analysis.
resultsThe expression of CCT3 was significantly suppressed by transduction with lentiviral shRNA; CCT3 knockdown significantly reduced the proliferation and metastasis ability of breast cancer cells (HCC 1937 and MDA-MB-231), increased the proportion of cells in S phase, and decreased the proportion of cells in G1 phase compared to those in shControl cells. There was no significant change in the number of cells in the G2/M phase. Apoptosis analysis showed that knockdown of CCT3 induced apoptosis in breast cancer cells. Western blot analysis showed that the expression of many signal transduction proteins was changed after suppression of CCT3. A rescue experiment showed that overexpression of NFκB-p65 rescued the cell proliferation and migration affected by CCT3 in breast cancer cells.
conclusionCCT3 is closely related to the proliferation and migration of breast cancer and may be a novel therapeutic target.
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