Xuedong Yin

1 Introduction Colorectal cancer (CRC) is the third most commonly diagnosed malignancy worldwide and a leading cause of cancer mortality (1). Although contemporary treatments—chemotherapy, surgical resection, targeted therapy, and immunotherapy—have improved survival, outcomes remain suboptimal because of marked intratumoral heterogeneity, therapeutic resistance, and the high recurrence of metastatic disease (2, 3).

Materials and methods Animals have been handled according to the National Institutes of Health guidelines. Animal testing was approved by the Board of Animal Ethics in Shanghai Children’s Hospital (2019R022-F01). Male C57BL/6 mice were obtained from Shanghai Model Organisms Center, Inc (Shanghai, China). All animals were housed in a temperature and light-dominated environment under 12: 12 light: dark circulation. All mice had free access to low-sodium diet (0.01% sodium diet) and water.

Abstract Vancomycin (VCM)-induced nephrotoxicity impedes its treatment applications. Thus, it is important to clarify the relevant mechanism. This study investigated phosphoprotein changes attributable to the VCM nephrotoxicity mechanisms. Biochemical, pathological and phosphoproteomic analyses based on C57BL/6 mice were performed to explore the mechanisms.VCM-treated mice showed increased levels of blood urea nitrogen and creatinine, and signs of acute tubular necrotic lesions.