IndraLab

Statements

EIF3H inhibits apoptotic process. 14 / 15
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"Our results are in agreement with previous reports suggesting that apoptosis of CRC cells was induced by EIF3H knockdown through upregulation of Bad, BAX, cleaved caspase-3, caspase9, cleaved PARP, and cytochrome C and downregulation of Bcl-2."
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"These results demonstrated that knockdown of EIF3H induced CRC cell apoptosis."
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"EIF3h potentiates the cell proliferation and inhibits the cell apoptosis of gastric cancer cells 13."
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"The results showed that silencing of EIF3H weakened cell growth and promoted apoptosis."
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"Flow cytometry showed that inhibition of EIF3H expression induced G0/G1 phase arrest and promote apoptosis in osteosarcoma cells."
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"EIF3H knockdown inhibited cell growth, migration, colony formation, and promoted apoptosis, and this was confirmed with GFP expressing infected cells that were counted daily for 5 days."
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"The knockdown of EIF3H, TPPP3, or DOCK2 promoted apoptosis of stem cells."
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"Furthermore, overexpressed eIF3h inhibits Myc dependent induction of apoptosis of primary prostate cells."
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"Overexpression of eIF3h has recently been shown to inhibit Myc dependent induction of apoptosis of primary prostate cells and EIF3H and MYC and may cooperate in enhanced protein translation either in a general way or for a specific subset of mRNAs XREF_BIBR."
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"XREF_BIBR Coamplification of EIF3H may also reduce MYC dependent apoptosis in prostate epithelial cells."
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"As shown in XREF_FIG, EIF3H knockdown also increased the rate of apoptosis in the two OS cell lines based on flow cytometry using Annexin V and 7-AAD double staining at both the early and late phases of apoptosis (Saos2 cells : 14.13 and 3.83% vs. 4.97 and 0.67% in controls, respectively, P < 0.05; U2OS cells : 7.96 and 12.53% vs. 6.89 and 7.14% in controls, respectively, P < 0.01)."
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"Mahmood et al demonstrated that EIF3H knockdown with specific small interfering RNA induced cell cycle arrest and apoptosis in breast tumour cells."
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"Thus, we come to the conclusion that EIF3H promotes proliferation and migration of iCCAs, inhibiting apoptosis of iCCA cells at the same time by stabilizing the CCND1 protein structure."
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"However, it was recently reported that overexpression of EIF3H inhibited Myc dependent induction of apoptosis in primary prostate cells, which suggests that EIF3H and MYC may cooperate to enhance protein translation [38]."
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