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RNAi-mediated knockdown of ?-enolase increases the sensitivity of tumor cells to antitubulin chemotherapeutics.

ABSTRACT: The over-expression of ?-enolase was demonstrated in several cancers, including lung, brain, breast, colon and prostate. In this report, we investigated the effects of ?-enolase knockdown on the sensitivity of cancer cells to chemotherapeutic drugs. RNAi-mediated knockdown of ?-enolase in A549 and H460 lung, MCF7 breast and CaOV3 ovarian cancer cells caused a significant increase in the sensitivity of these cells to antitubulin chemotherapeutics (e.g., vincristine and taxol), but not to doxorubicin, etoposide or cisplatinum. This is the first demonstration showing the effects of ?-enolase expression on the sensitivity of tumor cells to clinically relevant chemotherapeutics.

SUBMITTER: Georges E

PROVIDER: S-EPMC3242425 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature

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RNAi-mediated knockdown of α-enolase increases the sensitivity of tumor cells to antitubulin chemotherapeutics.

Georges Elias E Bonneau Anne-Marie AM Prinos Panagiotis P

International journal of biochemistry and molecular biology 20111021 4

The over-expression of α-enolase was demonstrated in several cancers, including lung, brain, breast, colon and prostate. In this report, we investigated the effects of α-enolase knockdown on the sensitivity of cancer cells to chemotherapeutic drugs. RNAi-mediated knockdown of α-enolase in A549 and H460 lung, MCF7 breast and CaOV3 ovarian cancer cells caused a significant increase in the sensitivity of these cells to antitubulin chemotherapeutics (e.g., vincristine and taxol), but not to doxorubi ...[more]

PMID: 22187664

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KLHL5 knockdown increases cellular sensitivity to anticancer drugs.

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[Small interfering RNA-mediated ?-enolase knockdown suppresses glycolysis and proliferation of human glioma U251 cells in vitro].

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