AI Article Synopsis
- HER2-overexpressing cancer cells show resistance to common chemotherapy drugs, cisplatin (CDDP) and doxorubicin (DXR).
- The SV40 T/t-common polypeptide can make these resistant cancer cells more sensitive to CDDP and DXR, leading to increased cell death (apoptosis).
- T/t-common works by inhibiting proteins Bcl-2 and Bcl-XL, and reducing ERK activity, suggesting that combining T/t-common with these chemotherapies could improve treatment outcomes for HER2-overexpressing cancers, as demonstrated in mouse models.
Article Abstract
HER2-overexpressing cancer cells are resistant to cisplatin (CDDP) and doxorubicin (DXR). Here we report that SV40 T/t-common polypeptide could specifically sensitize HER2-overexpressing cancer cells to CDDP and DXR and specifically enhance CDDP- or DXR-induced apoptosis in these cells. This activity of T/t-common may be attributed to its ability to inhibit Bcl-2 and Bcl-XL and to suppress ERK activity in CDDP- or DXR-treated HER2-overexpressing cancer cells. T/t-common could enhance the antitumor activity of DXR on HER2-overexpressing ovarian tumor in NOD/SCID mice, suggesting that combination therapy using T/t-common and chemotherapeutic agents may provide a new approach for treating HER2-overexpressing cancers.
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| http://dx.doi.org/10.1016/j.canlet.2012.04.019 | DOI Listing |
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