Radiotherapy is the first line treatment for small cell lung cancer (SCLC); However, radio-resistance accompanies with the treatment and hampers the prognosis for SCLC patients. The underlying mechanisms remains elusive. Here we discovered that self-inflicted DNA breaks exist in SCLC cells after radiation. Moreover, using nuclease siRNA screening combined with high-content ArrayScan™ cell analyzer, we identified that Ribonuclease ZC3H12A is required for the self-inflicted DNA breaks after radiation and for SCLC cell survival after DNA damage. ZC3H12A expression was increased in response to DNA damage and when ZC3H12A was knocked down, the DNA repair ability of the cells was impaired, as evidenced by decreased expression of the DNA damage repair protein BRCA1, and increased γH2AX at DNA damage sites. Colony formation assay demonstrates that ZC3H12A knocked down sensitized small cell lung cancer radiotherapy. Therefore, the Ribonuclease ZC3H12A regulates endogenous secondary breaks in small cell lung cancer and affects DNA damage repair. ZC3H12A may act as an important radiotherapy target in small cell lung cancer.
Keyphrases
- dna damage
- small cell lung cancer
- dna repair
- oxidative stress
- induced apoptosis
- early stage
- single cell
- circulating tumor
- radiation induced
- brain metastases
- poor prognosis
- cell therapy
- radiation therapy
- cell free
- single molecule
- dna damage response
- newly diagnosed
- squamous cell carcinoma
- binding protein
- cell death
- signaling pathway
- transcription factor
- circulating tumor cells
- nucleic acid
- patient reported outcomes
- cell proliferation
- endoplasmic reticulum stress