Anti-apoptotic role of peroxiredoxin III in cervical cancer cells

After successful knockdown of PrxIII expression by small interfering RNA, we evaluated reactive oxygen species level, viable cell number, and apoptosis of cervical cancer cells along with the culture time

Lianqin Li; Yong-Gang Zhang; Chun-Ling Chen


Scholarcy highlights

  • As an energy-provider for cellular activities, mitochondrion is a major source of reactive oxygen species production
  • Among the 10 patients with stage IA cervical cancer, six cases were successfully cultured for both cancerous cells and adjacent normal epithelia
  • As shown in Fig. 1(A), PrxIII expression in cancer cells was significantly down-regulated after small interfering RNA
  • Other Prx members were significantly up-regulated after knockdown of PrxIII expression). quantitative real-time PCR analysis recognized that the up-regulated Prx members included PrxI, PrxII, and PrxV
  • Since most of chemotherapy or radiotherapy for cancers is through ROS increase and apoptotic induction, our results have provided a clue that PrxIII may be involved in the chemotherapeutic resistance of cervical cancer
  • Combining the present study with previous reports of PrxIII overexpression in cervical cancer, we conclude that PrxIII is an important regulator of intracellular ROS, which provides a favorable microenvironment for tumor growth and protects against oxidationinduced apoptosis
  • Our results have provided a new clue to the understanding of the mechanism for tumor progression or recurrence

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