radiosensitivity   4

Inhibition of Notch signaling pathway enhanced the radiosensitivity of breast cancer cells - Peng - 2018 - Journal of Cellular Biochemistry - Wiley Online Library
4Gy induced NOTCH1 protein and activation in MCF7/T47D as well as invasion. No analysis of ligands. Possibly look at radiation effects on macrophages?

This study aimed to investigate the effect of inhibiting the Notch signaling pathway on the radiosensitivity of breast cancer cells. Human breast cancer cell lines (MCF‐7 and T47D) were selected and treated with radiation of different doses. Cells were treated with Gamma secretase inhibitor (GSI) to analyze the effects of GSI on the Notch signaling, which were detected by Immunofluorescence assay, RT‐qPCR, and Western blot analysis. Besides, Transwell assay, Scratch test, colony formation assay, MTT assay, and flow cytometry were conducted to show the effects of GSI on the invasion and migration, survival fraction, cell viability, and apoptosis of MCF‐7 and T47D cells after radiation therapy. Moreover, cell transfection with a dominant negative mutant of RBPJ, the key transcription factor of Notch signaling pathway, were also applied to show the inhibition of Notch signaling pathway. Initially, we found that the 4 Gy radiation activated Notch signaling pathway, and enhanced the invasion and migration of MCF‐7 and T47D cells. However, GSI inhibited the Notch signaling pathway, and reversed the enhancement of radiation on the migration and invasion, promoted the enhancement of apoptosis and inhibition of proliferation of MCF‐7 and T47D cells induced by radiation. Except that, we also determined that GSI and dnRBPJ suppressed the upregulation of Notch signaling after radiation therapy. Our study demonstrated that inhibition of the Notch signaling pathway enhanced the radiosensitivity of breast cancer cells, which may provide evident for a beneficial adjuvant therapy in the breast cancer treatment.
Notch  radiation  radiosensitivity  MCF-7  T47D  GSI  invasion 
february 2019 by Segalllab
Knockdown of Cathepsin L promotes radiosensitivity of glioma stem cells both in vivo and in vitro
Useful paper, though only works with their own lines. Show that CTSL expression correlates with tumor grade and that CTSL/CD133 are more resistant to radiotherapy - might be interesting to check KIF9 KD sensitivity. " Our results have shown that the two glioma stem cell lines secreting high levels of Cathepsin L and CD133 have become more resistant to radiotherapy, while knockdown of Cathepsin L enhanced radiosensitivity with a dramatic reduction of CD133 expression both in vivo and in vitro. "
ctsl  glioblastoma  stem_cells  radiosensitivity  cd133 
september 2016 by Segalllab
Acta Pharmacologica Sinica - Inhibition of cathepsin L sensitizes human glioma cells to ionizing radiation in vitro through NF-[kappa]B signaling pathway
using U251 cells, see KD or inhibition of CTSL1 reduces nfkb induction and increases sensitivity to ionizing radiation, no other mechanism suggested.
u251  ctsl1  nfkb  radiosensitivity 
july 2016 by Segalllab
miR-375 Modulates Radiosensitivity of HR-HPV-Positive Cervical Cancer Cells by Targeting UBE3A through the p53 Pathway. - PubMed - NCBI
miR-375 expression was significantly lower in cervical cancer patients and radioresistant patients. In high-risk-HPV (+) cervical cancer cells, overexpression of miR-375 resulted in radiosensitivity at 4, 6, 8 Gy (similar to our results with UMSCC1 cells). There was also more active caspase 3 cell proportion of miR-375 overexpressing cells treated with 8Gy radiation. showed the miR-375 targets UBE3A. Knockdown of UBE3A significantly reduced cell proliferation.
mir-375  cervical  cancer  ube3a  radiosensitivity 
august 2015 by Segalllab

related tags

cancer  cd133  cervical  ctsl  ctsl1  glioblastoma  gsi  invasion  mcf-7  mir-375  nfkb  notch  radiation  stem_cells  t47d  u251  ube3a 

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