Vitamin D Enhances Radiosensitivity of Colorectal Cancer by Reversing Epithelial-Mesenchymal Transition
Front Cell Dev Biol. 2021 Aug 4;9:684855. doi: 10.3389/fcell.2021.684855
Xinyue Yu 1, Qian Wang 1, Baocai Liu 1, Ning Zhang 1, Guanghui Cheng 1
If have a high level of Vitamin D, sometimes the doctor can use less radio/chemo therapy
Less therapy ==> potentially decreased: hair loss, pain, appetite loss, gut problems, sleep loss, fatigue, etc.
Some chemotherapies also lower the vitamin D levels, so vitamin D levels need to be restored
Warning: Not reducing some cancer therapies when having a high level of vitamin D can be DEADLY
click on chart for details
- Vitamin D, Gut Microbiota, and Chemo-radiation interactions – Dec 2019
- Chemotherapy hair loss – prevented or treated by Vitamin D, US patent application – Nov 2019
- Topical - applied to the scalp: 4,000 IU – 7,200 IU; 5th patent on Chemo and Vitamin D
- Chemotherapy drugs often reduce Vitamin D levels, restoring levels helps– Aug 2018
- Cancer - after diagnosis pages containing RADIATION in VitaminDWiki title (7 as of Oct 2021)
Breast Cancer specific
- Vitamin D prevents breast cancer, reduces BC mortality, and reduces BC chemotherapy problems – Sept 2018
- Breast Cancer chemotherapy 2.7 X more likely to be successful if not vitamin D deficient – Dec 2017
Vitamin D Receptor is also important
Download the PDF from VitaminDWiki
Table of contents
Abstract
Colorectal cancer (CRC) is often resistant to conventional therapies. Previous studies have reported the anticancer effects of vitamin D in several cancers, its role in radiotherapy (RT) remains unknown. We found that 1α, 25-dihydroxyvitamin D3 (VD3), the biologically active form of vitamin D, had antitumor effect on CRC and sensitized CRC cells to ionizing radiation (IR). VD3 demonstrated synergistic effect in combination with IR, which were detected by colony formation and cell proliferation assay. Radiosensitivity restoration induced by VD3 was associated with a series of phenotypes, including apoptosis, autophagy, and epithelial-mesenchymal transition (EMT). Using proteomics, "regulation of cell migration" and "cadherin" were found to be obviously enriched GO terms. Moreover, cystatin D and plasminogen activator inhibitor-1 (PAI-1), the differentially expressed proteins, were associated with EMT. Next, we confirmed the contributions of these two genes in enhancing IR sensitivity of CRC cells upon inhibition of EMT. As determined by proteomics, the mechanism underlying such sensitivity involved partially block of JAK/STAT3 signaling pathway. Furthermore, VD3 also elicited sensitization to RT in xenograft CRC models without additional toxicity.
Our study revealed that VD3 was able to act in synergy with IR both in vitro and in vivo and could also confer radiosensitivity by regulating EMT, thereby providing a novel insight for elevating the efficacy of therapeutic regimens.
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