When ER-α was blocked in liver cancer cells, fewer cells were in the DNA-copying phase and more cells died, which explains why the cells grew slower.
Scientific Claim
In Hep3B and HCCLM3 human hepatocellular carcinoma cell lines, ER-α knockdown resulted in a significant decrease in S-phase cell cycle distribution (P < 0.05) and increased apoptosis rates (P < 0.05), suggesting a mechanism for reduced proliferation.
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
definitive
Can make definitive causal claims
Assessment Explanation
The study directly measured cell cycle and apoptosis effects and interpreted them as the mechanism for reduced proliferation. The claim accurately describes the observed relationship without overgeneralizing to humans.
Source Excerpt
“Compared with cells in the other groups, cells infected with ER-α siRNA group showed a substantial decrease in S-phase (P < 0.05, resp.) (Figure 3(a)). We also carried out an Annexin V Apoptosis Assay to determine the apoptotic effect of ER-α siRNA on Hep3B and HCCLM3 cells. In time course experiment, silencing of ER-α significantly increased the percentage of apoptotic cells compared with the other groups (P < 0.05, resp.) (Figure 3(b)). These results indicated that ER-α knockdown inhibited HCC cell proliferation by inducing cell cycle arrest and apoptosis.”
Evidence from Studies
Supporting Evidence (1)
The study directly measured cell cycle distribution and apoptosis rates, and the authors interpreted these findings as explaining the mechanism behind reduced proliferation. The statistical significance (P < 0.05) supports the causal relationship between ER-α knockdown and these cellular changes.
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