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Vitamin B consists of a group of water-soluble micronutrients that are mainly derived from the daily diet. They serve as cofactors, mediating multiple metabolic pathways in humans. As an integrated part of human health, gut microbiota could produce, consume, and even compete for vitamin B with the host. The interplay between gut microbiota and the host might be a crucial factor affecting the absorbing processes of vitamin B. On the other hand, vitamin B supplementation or deficiency might impact the growth of specific bacteria, resulting in changes in the composition and function of gut microbiota. Together, the interplay between vitamin B and gut microbiota might systemically contribute to human health. In this review, we summarized the interactions between vitamin B and gut microbiota and tried to reveal the underlying mechanism so that we can have a better understanding of its role in human health.

Radiation-induced lung injury (RILI) is a common serious complication and dose-limiting factor caused by radiotherapy for lung cancer. This study was to investigate radioprotective effects of grape seed proanthocyanidins (GSP) on normal lung as well as radiosensitizing effects on lung cancer. In vitro , we demonstrated radioprotective effects of GSP on normal alveolar epithelial cells (MLE-12 and BEAS/2B) and radiosensitizing effects on lung cancer cells (LLC and A549). In vivo , we confirmed these two-way effects in tumor-bearing mice. The results showed that GSP inhibited tumor growth, and played a synergistic killing effect with radiotherapy on lung cancer. Meanwhile, GSP reduced radiation damage to normal lung tissues. The two-way effects related to the differential regulation of the MAPK signaling pathway by GSP on normal lung and lung cancer. Moreover, GSP regulated secretion of cytokines IL-6 and IFN-γ and expression of p53 and Ki67 on normal lung and lung cancer. Our findings suggest that GSP is expected to be an ideal radioprotective drug for lung cancer patients who are treated with radiotherapy.

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Background Neoadjuvant chemoradiotherapy is a standard treatment for locally advanced rectal cancer; however, resistance to chemoradiotherapy is one of the main obstacles to improving treatment outcomes. The goal of this study was to explore the role of PRDM15 involved in the radioresistance of colorectal cancer and to clarify the underlying mechanism. Methods The expression and localization of PRDM15 was measured with Western blot and immunofluorescence assay. Lenti-virus was applied to perform knockdown or overexpression of PRDM15. Colorectal cancer cells exposed to γ-rays were assayed by DNA damage, cytotoxicity, apoptosis and cell cycle. Moreover, DNA damage response was detected and immunoprecipitation was used to explore protein interactions. The potent role of PRDM15 in overcoming radioresistance was investigated in CDX and PDX models. Finally, the correlation between PRDM15 expression and clinical outcomes were investigated in 80 locally advanced rectal cancer patients receiving neoadjuvant chemoradiotherapy. Results After DNA damage, PRDM15 was upregulated and localized to DNA damage sites, colocalized with γH2AX. Knockdown of PRDM15 inhibited DNA damage repair and increased radiosensitivity in colorectal cancer cells. Mechanistically, PRDM15 promoted DNA repair by interacting with DNA-PKcs and Ku70/Ku80 complex. Knockdown of PRDM15 sensitized CDX and PDX models to radiotherapy. Higher PRDM15 expression in cancer tissue was associated with inferior tumor regression and poorer prognosis in colorectal cancer patients treated with neoadjuvant chemoradiotherapy. Conclusions Our findings revealed that inhibiting PRDM15 was potent to overcome radioresistance through abrogating DNA repair in colorectal cancer cells. Additionally, the expression level of PRDM15 could be applied to predict radiotherapy responsiveness in rectal cancer patients.