ArticleOncotarget2016
Pre-clinical characterization of PKC412, a multi-kinase inhibitor, against colorectal cancer cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Targeting POLRMT by IMT1 inhibits colorectal cancer cell growth.Cell death & disease · 2024Article
- The sphingosine kinase 2 inhibitor ABC294640 inhibits cervical carcinoma cell growth.Oncotarget · 2018Article
- Dual inhibition of BRD4 and PI3K-AKT by SF2523 suppresses human renal cell carcinoma cell growth.Oncotarget · 2017Article
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- ERK inhibition sensitizes CZ415-induced anti-osteosarcoma activityOncotarget · 2017Article
- DlgR2 knockdown boosts dendritic cell activity and inhibits hepatocellular carcinoma tumorOncotarget · 2017Article
- Identification of DNA-PKcs as a primary resistance factor of TIC10 in hepatocellular carcinoma cells.Oncotarget · 2017Article
- AMPK-autophagy inhibition sensitizes icaritin-induced anti-colorectal cancer cell activity.Oncotarget · 2017Article
- Article
- CC-223 blocks mTORC1/C2 activation and inhibits human hepatocellular carcinoma cells in vitro and in vivo.PloS one · 2017Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The potential effect of PKC412, a small molecular multi-kinase inhibitor, in colorectal cancer (CRC) cells was evaluated here. We showed that PKC412 was cytotoxic and anti-proliferative against CRC cell lines (HT-29, HCT-116, HT-15 and DLD-1) and primary CRC cells. PKC412 provoked caspase-dependent apoptotic death, and induced G2-M arrest in the CRC cells. AKT activation was inhibited by PKC412 in CRC cells. Reversely, expression of constitutively-active AKT1 (CA-AKT1) decreased the PKC412's cytotoxicity against HT-29 cells. We propose that Bcl-2 could be a primary resistance factor of PKC412. ABT-737, a Bcl-2 inhibitor, or Bcl-2 siRNA knockdown, dramatically potentiated PKC412's lethality against CRC cells. Forced Bcl-2 over-expression, on the other hand, attenuated PKC412's cytotoxicity. Significantly, PKC412 oral administration suppressed AKT activation and inhibited HT-29 tumor growth in nude mice. Mice survival was also improved with PKC412 administration. These results indicate that PKC412 may have potential value for CRC treatment.
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