Objective This study aimed to explore the association of integrin α7 with clinicopathological characteristics and overall survival (OS) in clear cell renal cell carcinoma (ccRCC) patients. Methods 179 ccRCC patients who underwent nephrectomy were included in this retrospective study. Tumor tissue and paired adjacent tissue specimens of patients were obtained. Immunohistochemistry assay was performed to detect integrin α7 expression. OS was calculated with the median follow‐up duration of 91.0 months (range: 3.0‐116.0 months). Results Integrin α7 was highly expressed in tumor tissue compared to paired adjacent tissue (P < .001), and tumor integrin α7 high expression was correlated with higher pathological grade (P = .004), increased T stage (P = .017), and advanced TNM stage (P = .033). Kaplan–Meier curve showed that patients with integrin α7 high expression (mean OS = 69.8, 95%CI: 60.5‐79.1 months) presented with worse OS compared to patients with integrin α7 low expression (mean OS = 101.8, 95%CI: 96.0‐107.7 months; P < .001). Multivariate Cox's regression analysis further disclosed that tumor integrin α7 high expression independently predicted poor OS (P < .001). Conclusion Integrin α7 is upregulated and correlates with higher pathological grade, increased T stage, and advanced TNM stage, meanwhile it also acts as a valuable prognostic factor for worse survival in ccRCC patients.

Obesity significantly impacts living a normal life by increasing morbidity. Additionally, obesity has been shown to be closely associated with severe inflammation in adipocytes. It is widely reported that berberine (BBR) has an anti-inflammatory effect and can reduce glucose and lipid accumulation, whereas ginsenoside Rb1 (Rb1) has been shown to have a significant inhibitory effect on insulin resistance and lipid peroxidation. In this study, we aimed to explore the synergetic effect of BBR and Rb1 on tumor necrosis factor alpha (TNF-α)-treated adipocytes and the mechanisms underlying it. We found that TNF-α reduced cell viability, facilitated the production of inflammatory factors, induced adipogenesis, activated the nuclear factor kappa B (NF-κB) pathway, and increased the expression of peroxisome proliferator-activated receptor gamma, CCAAT enhancer-binding protein alpha, and sterol regulatory element-binding protein-1 c in adipocytes. However, these effects were significantly alleviated by BBR or Rb1. Additionally, a synergetic effect was observed when BBR and Rb1 were used in combination. The effects of BBR in combination with Rb1 on cell proliferation, inflammation, adipogenesis, and the NF-κB pathway in TNF-α-treated adipocytes were significantly abolished by receptor activator of nuclear factor kappa-Β ligand, which is an activator of the NF-κB pathway. Collectively, the results revealed that BBR and Rb1 have a synergetic protective effect against TNF-α-induced inflammation in adipocytes. The mechanism underlying this synergetic effect was found to be inhibition of the NF-κB signaling pathway.

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