As a major part of corporate social responsibility (CSR) practices, Chinese companies have emphasized employee satisfaction to achieve sustainable development. However, it is still unclear how employees perceive organizational CSR efforts and whether such perceptions bring employee satisfaction and loyalty. To answer these timely inquires, we developed and empirically tested a theoretical framework modeling employee satisfaction as both mediator and moderator on the relationship between employee perception of organizational CSR efforts and their loyalty to enterprises. Based on 438 usable questionnaires collected from four typical companies, we found that solely providing money-related welfare and improving the working environment can be detrimental to employee loyalty, but by increasing employee satisfaction of personal treatment, companies can mitigate such a side-effect. Employee satisfaction of personal treatment and general company effort are necessary to enhance their affective commitment.

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Background: RNA modification is one of the epigenetic mechanisms that regulates post-transcriptional gene expression, and abnormal RNA modifications have been reported to play important roles in tumorigenesis. N7-methylguanosine (m7G) is an essential modification at the 5′ cap of human mRNA. However, a systematic and pan-cancer analysis of the clinical relevance of m7G related regulatory genes is still lacking.Methods: We used univariate Cox model and Kaplan-Meier analysis to generate the forest plot of OS, PFI, DSS and identified the correlation between the altered expression of m7G regulators and patient survival in 33 cancer types from the TCGA and GTEx databases. Then, the “estimate” R-package, ssGSEA and CIBERSORT were used to depict the pan-cancer immune landscape. Through Spearman’s correlation test, we analyzed the correlation between m7G regulators and the tumor microenvironment (TME), immune subtype, and drug sensitivity of the tumors, which was further validated in NSCLC. We also assessed the changes in the expression of m7G related regulatory genes in NSCLC with regards to the genetic and transcriptional aspects and evaluated the correlation of METTL1 and WDR4 expression with TMB, MSI and immunotherapy in pan-cancer.Results: High expression of most of the m7G regulators was significantly associated with worse prognosis. Correlation analyses revealed that the expression of majority of the m7G regulators was correlated with tumor immune infiltration and tumor stem cell scores. Drug sensitivity analysis showed that the expression of CYFP1,2 was closely related to drug sensitivity for various anticancer agents (p < 0.001). Analysis of the pan-cancer immune subtype revealed significant differences in the expression of m7G regulators between different immune subtypes (p < 0.001). Additionally, the types and proportions of mutations in METTL1 and WDR4 and their relevance to immunotherapy were further described.Conclusion: Our study is the first to evaluate the correlation between the altered expression of m7G regulators and patient survival, the degree of immune infiltration, TME and drug sensitivity in pan-cancer datasets.

Dabrafenib is a novel small molecule tyrosine kinase inhibitor (TKI) which is used to treat metastatic melanoma. The aim of this research was to survey the effects of dabrafenib on human UDP‐glucuronosyltransferases (UGTs) and to evaluate the risk of drug–drug interactions (DDIs). The formation rates for 4‐methylumbelliferone (4‐MU) glucuronide and trifluoperazine‐glucuronide in 12 recombinant human UGT isoforms with or without dabrafenib were measured and HPLC was used to investigate the inhibitory effects of dabrafenib on UGTs. Inhibition kinetic studies were also conducted. In vitro–in vivo extrapolation approaches were further used to predict the risk of DDI potentials of dabrafenib via inhibition of UGTs. Our data indicated that dabrafenib had a broad inhibitory effect on 4‐MU glucuronidation by inhibiting the activities of UGTs, especially on UGT1A1, UGT1A7, UGT1A8, and UGT1A9, and dabrafenib could increase the area under the curve of co‐administered drugs. Dabrafenib is a strong inhibitor of several UGTs and the co‐administration of dabrafenib with drugs primarily metabolized by UGT1A1, 1A7, 1A8 or 1A9 may induce potential DDIs.