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HSP60, a protein downregulated by IGFBP7 in colorectal carcinoma
Wenjing Ruan1, Yinghong Wang, Yu Ma
1Department of Pathology, School of Medicine, Zhejiang University, 388 Yuhangtang Road, Hangzhou 310058, Zhejiang Province, China.
Background:
In our previous study, it was well defined that IGFBP7 was an important tumor suppressor gene in colorectal cancer (CRC). We aimed to uncover the downstream molecules responsible for IGFBP7's behaviour in this study.
Methods:
Differentially expressed protein profiles between PcDNA3.1(IGFBP7)-transfected RKO cells and the empty vector transfected controls were generated by two-dimensional gel electrophoresis (2-DE) and mass spectrometry (MS) identification. The selected differentially expressed protein induced by IGFBP7 was confirmed by western blot and ELISA. The biological behaviour of the protein was explored by cell growth assay and colony formation assay.
Results:
Six unique proteins were found differentially expressed in PcDNA3.1(IGFBP7)-transfected RKO cells, including albumin (ALB), 60 kDa heat shock protein(HSP60), Actin cytoplasmic 1 or 2, pyruvate kinase muscle 2(PKM2), beta subunit of phenylalanyl-tRNA synthetase(FARSB) and hypothetical protein. The downregulation of HSP60 by IGFBP7 was confirmed by western blot and ELISA. Recombinant human HSP60 protein could increase the proliferation rate and the colony formation ability of PcDNA3.1(IGFBP7)-RKO cells.
Conclusion:
HSP60 was an important downstream molecule of IGFBP7. The downregulation of HSP60 induced by IGFBP7 may be, at least in part, responsible for IGFBP7's tumor suppressive biological behaviour in CRC.
Insights
Insulin-like growth factor-binding protein 7 (IGFBP7) acts as a tumor suppressor in colorectal cancer (CRC). This study identified heat shock protein 60 (HSP60) as a key downstream molecule, whose downregulation by IGFBP7 contributes to its tumor-suppressive effects in CRC.
Area of Science:
- Molecular Biology
- Cancer Research
- Genetics
Background:
- Previous research established Insulin-like growth factor-binding protein 7 (IGFBP7) as a crucial tumor suppressor gene in colorectal cancer (CRC).
- This study aimed to elucidate the downstream molecular mechanisms underlying IGFBP7's tumor-suppressive functions in CRC.
Purpose of the Study:
- To identify downstream molecules regulated by IGFBP7 in colorectal cancer cells.
- To investigate the functional role of identified downstream molecules in mediating IGFBP7's tumor suppressor activity.
Main Methods:
- Proteomic analysis using two-dimensional gel electrophoresis (2-DE) and mass spectrometry (MS) to compare IGFBP7-transfected RKO cells with controls.
- Validation of differentially expressed proteins via Western blot and ELISA.
- Functional assays including cell growth and colony formation assays to assess the biological impact of identified proteins.
Main Results:
- Six proteins were found to be differentially expressed, including heat shock protein 60 (HSP60).
- IGFBP7 significantly downregulated HSP60 expression, confirmed by Western blot and ELISA.
- Exogenous addition of HSP60 protein promoted proliferation and colony formation in IGFBP7-expressing RKO cells.
Conclusions:
- Heat shock protein 60 (HSP60) is identified as a significant downstream effector of IGFBP7 in colorectal cancer.
- The observed downregulation of HSP60 by IGFBP7 is a key mechanism contributing to IGFBP7's tumor-suppressive role in CRC progression.
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