Effects of peroxidoxin 1 on apoptosis of undifferentiated thyroid cancer FRO cells mediated by proteasome inhibitors
Hua‐Qin Wang
Abstract
Hua‐Qin Wang
Abstract
OBJECTIVE:To investigate the role of peroxidoxin 1 (Prx1) in thyroid cancer cell death induced by proteasome inhibitors. MESUTLS: The undifferentiated thyroid cancer FRO cells were treated with vehicle,proteasome inhibitor MG132,PSI and lactacystin; Prx1 expression levels were knockdown by RNA interference (RNAi); Prx1 mRNA and protein levels were analyzed by using real-time RT-PCR and Western blot,respectively; the apoptotic rate was analyzed by using flow cytometry (FCM). RESULTS: MG132,PSI and lactacystin significantly increased the mRNA and protein levels of Prx1 (P0.01) in undifferentiated thyroid cancer FRO cells; small interfering RNA against Prx1 (siPrx1) markedly reduced the Prx1 mRNA and protein levels when compared with vehicle or scramble siRNA (P0.01),in addition,siPrx1 dramatically increased MG132-,PSI- or lactacystin-mediated increase in apoptotic cells (P0.01). CONCLUSION: Proteasome inhibitors increase the Prx1 expression in undifferentiated thyroid cancer FRO cells,and the suppression of Prx1 expression by siPrx1 significantly enhances the apoptosis of FRO cells induced by proteasome inhibitors.
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OBJECTIVE:To investigate the role of peroxidoxin 1 (Prx1) in thyroid cancer cell death induced by proteasome inhibitors. MESUTLS: The undifferentiated thyroid cancer FRO cells were treated with vehicle,proteasome inhibitor MG132,PSI and lactacystin; Prx1 expression levels were knockdown by RNA interference (RNAi); Prx1 mRNA and protein levels were analyzed by using real-time RT-PCR and Western blot,respectively; the apoptotic rate was analyzed by using flow cytometry (FCM). RESULTS: MG132,PSI and lactacystin significantly increased the mRNA and protein levels of Prx1 (P0.01) in undifferentiated thyroid cancer FRO cells; small interfering RNA against Prx1 (siPrx1) markedly reduced the Prx1 mRNA and protein levels when compared with vehicle or scramble siRNA (P0.01),in addition,siPrx1 dramatically increased MG132-,PSI- or lactacystin-mediated increase in apoptotic cells (P0.01). CONCLUSION: Proteasome inhibitors increase the Prx1 expression in undifferentiated thyroid cancer FRO cells,and the suppression of Prx1 expression by siPrx1 significantly enhances the apoptosis of FRO cells induced by proteasome inhibitors.
Key concepts: Lactacystin, MG132, Proteasome inhibitor, Gene knockdown, Proteasome, Apoptosis, Cancer research, Thyroid cancer