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<p>Radioresistance of adenocarcinoma cells limits the efficiency of radiotherapy. In addition to the cell nucleus, ionizing radiation (IR) also induces damage to the mitochondria. Mitophagy, a selective degradation of impaired mitochondria via autophagy, has been found to respond to IR, but its role in the radiosensitivity of adenocarcinoma cells remains unclear. Using several different adenocarcinoma cell lines, we confirmed that exposing the adenocarcinoma cells to 5&#xa0;Gy X-ray enhanced the expression of some mitophagy receptors and increased mitophagy activity. However, pharmacological inhibition of mitophagy by mdivi-1 did not significantly change the radiosensitivity of HCT116 and A549 cells. Similarly, molecular targeting inhibition of mitophagy by BNIP3L knockdown in HCT116 and A549 cells that showed significant IR-induced BNIP3L up-regulation did also not significantly affect the radiosensitivity of adenocarcinoma cells, although the IR-induced enhancement of mitophagy activity was effectively suppressed. According to our data, mitophagy is responsible to IR but plays a very limited role in the radiosensitivity of adenocarcinoma cells. Further in vivo studies are warranted to elucidate the radiosensitizing effect of targeting mitophagy on malignant tumors.</p>

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Mitophagy is responsible to ionizing radiation but plays a very limited role in the radiosensitivity of adenocarcinoma cells

  • 期刊论文

  • 发表日期：

    2025年11月21日

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  • Chen Yan,
  • Kai Huang,
  • Yong Xu,
  • Wei-Hang Lu,
  • Jing Cai,
  • Tao-Sheng Li

摘要

Radioresistance of adenocarcinoma cells limits the efficiency of radiotherapy. In addition to the cell nucleus, ionizing radiation (IR) also induces damage to the mitochondria. Mitophagy, a selective degradation of impaired mitochondria via autophagy, has been found to respond to IR, but its role in the radiosensitivity of adenocarcinoma cells remains unclear. Using several different adenocarcinoma cell lines, we confirmed that exposing the adenocarcinoma cells to 5 Gy X-ray enhanced the expression of some mitophagy receptors and increased mitophagy activity. However, pharmacological inhibition of mitophagy by mdivi-1 did not significantly change the radiosensitivity of HCT116 and A549 cells. Similarly, molecular targeting inhibition of mitophagy by BNIP3L knockdown in HCT116 and A549 cells that showed significant IR-induced BNIP3L up-regulation did also not significantly affect the radiosensitivity of adenocarcinoma cells, although the IR-induced enhancement of mitophagy activity was effectively suppressed. According to our data, mitophagy is responsible to IR but plays a very limited role in the radiosensitivity of adenocarcinoma cells. Further in vivo studies are warranted to elucidate the radiosensitizing effect of targeting mitophagy on malignant tumors.