Complement factor H‑related 3 overexpression affects hepatocellular carcinoma proliferation and apoptosis
- Hong Liu
- Ligang Zhang
- Pengyan Wang
Published online on: July 23, 2019
Copyright: © Liu et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
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Complement factor H‑related 3 (CFHR3) belongs to the human factor H protein family and is associated with various human diseases, including nephropathy, age‑related macular degeneration and atypical hemolytic uremic syndrome. However, to the best of our knowledge, the role of CFHR3 in hepatocellular carcinoma (HCC) remains largely unknown. In the present study, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis were performed to determine mRNA and protein expression levels of CFHR3 in HCC and normal adjacent tissue. In addition, CFHR3 was overexpressed in Huh‑7 cells and cell counting kit‑8 assay was used to determine cell viability. Cell proliferation and apoptosis were assessed using flow cytometry, RT‑qPCR and western blotting. The results demonstrated that mRNA (2‑ΔΔCq) and protein expression levels of CFHR3 were significantly lower in tumor tissue compared with in adjacent tissue. Additionally, CFHR3 overexpression decreased cell viability, inhibited cell proliferation and significantly increased apoptosis. It was also identified that CFHR3 could downregulate the expression of Ki67. The results suggested that CFHR3 induced apoptosis by downregulating the expression of survivin and B cell lymphoma 2, upregulating the expression of Bcl‑2‑associated X and promoting caspase‑3 activity. Western blotting revealed that CFHR3 significantly inhibited the protein expression levels of phosphorylated (p)‑phosphoinositide 3‑kinase (PI3K), p‑protein kinase B (Akt) and p‑mammalian target of rapamycin (mTOR). Overexpression of CFHR3 suppressed proliferation and promoted apoptosis of HCC cells by inhibiting the PI3K/Akt/mTOR signaling pathway.