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Published on: March 26, 2018
Effects of parafibromin expression on the phenotypes and relevant mechanisms in the DLD-1 colon carcinoma cell line
Shuang Zhao1, Hong-Zhi Sun, Shi-Tu Zhu
1Cancer Research Center, The First Affiliated Hospital of Liaoning Medical University, JinZhou, China. zheng_huachuan @hotmail.com
Background:
Parafibromin is a protein encoded by the HRPT2 (hyperparathyroidism 2) oncosuppressor gene and its down-regulated expression is involved in pathogenesis of parathyroid, breast, gastric and colorectal carcinomas. This study aimed to clarify the effects of parafibromin expression on the phenotypes and relevant mechanisms of DLD-1 colon carcinoma cells.
Methods:
DLD-1 cells transfected with a parafibromin-expressing plasmid were subjected to examination of phenotype, including proliferation, differentiation, apoptosis, migration and invasion. Phenotype-related proteins were measured by Western blot. Parafibromin and ki-67 expression was detected by immunohistochemistry on tissue microarrays.
Results:
The transfectants showed higher proliferation by CCK-8, better differentiation by electron microscopy and ALP activity and more apoptotic resistance to cisplatin by DNA fragmentation than controls. There was no difference in early apoptosis by annexin V, capase-3 activity, migration and invasion between DLD-1 cells and their transfectants. Ectopic parafibromin expression resulted in down-regulated expression of smad4, MEKK, GRP94, GRP78, GSK3β-ser9, and Caspase-9. However, no difference was detectable in caspase-12 and -8 expression. A positive relationship was noted between parafibromin and ki-67 expression in colorectal carcinoma.
Conclusions:
Parafibromin overexpression could promote cell proliferation, apoptotic resistance, and differentiation of DLD-1 cells.
Insights
Parafibromin overexpression enhances colon cancer cell proliferation, differentiation, and resistance to apoptosis. This study investigated its effects on DLD-1 cells, revealing impacts on key cellular mechanisms.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Parafibromin, encoded by the HRPT2 tumor suppressor gene, is downregulated in various carcinomas.
- Reduced parafibromin expression is implicated in parathyroid, breast, gastric, and colorectal cancer development.
Purpose of the Study:
- To investigate the impact of parafibromin expression on the phenotypic characteristics of DLD-1 colon carcinoma cells.
- To elucidate the underlying molecular mechanisms influenced by parafibromin in colon cancer cells.
Main Methods:
- DLD-1 cells were transfected with a parafibromin-expressing plasmid.
- Phenotypic analyses included proliferation, differentiation, apoptosis, migration, and invasion assays.
- Protein expression levels (e.g., smad4, MEKK, GRP94, GRP78, GSK3β-ser9, Caspase-9) were assessed via Western blot; parafibromin and ki-67 expression were evaluated by immunohistochemistry.
Main Results:
- Overexpression of parafibromin led to increased cell proliferation, enhanced differentiation, and greater resistance to cisplatin-induced apoptosis.
- No significant changes were observed in early apoptosis, caspase-3 activity, migration, or invasion.
- Parafibromin overexpression downregulated key proteins including smad4, MEKK, GRP94, GRP78, GSK3β-ser9, and Caspase-9.
Conclusions:
- Parafibromin overexpression promotes colon cancer cell proliferation and differentiation.
- Elevated parafibromin levels enhance cellular resistance to apoptosis.
- The study identified specific molecular pathways affected by parafibromin in colon carcinoma.
