Epidemiology of Renal Cell Carcinoma

Sánchez, Alejandro; Allard, Christopher B.; Wilson, Kathryn M.

doi:10.1007/978-3-319-35153-7_17

Cited by 1 publication

(2 citation statements)

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“…The incidence of RCC is increasing year by year and there are significantly more male patients than female patients. 1,2 Cigarette smoke (CS) has been recognized as one of the most important risk factors of RCC development and numerous epidemiological studies have revealed that CS exposure can promote the initiation and progression of RCC. 15,16 Tobacco contains a variety of carcinogens, and their combustion products can attack cells through various mechanisms, consequently activating signaling pathways related to each tumor in a network, leading to the rapid development of tumors.…”

Section: Discussionmentioning

confidence: 99%

“…Epidemiological investigations found that over 90% of renal cancers are renal cell carcinoma, and 50% of renal cancer in patients is associated with long-term smoking. 1,2 Although cigarette smoke (CS) shows tight correlation with renal tumor occurrence and progression, few studies have examined the mechanisms by which CS is involved in renal carcinoma progression at molecular level. Consequently, the current research aimed to investigate CS pathogenesis in renal cell carcinoma at molecular level.…”

Section: Introductionmentioning

confidence: 99%

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<p>Curcumin Negatively Regulates Cigarette Smoke-Induced Renal Cell Carcinoma Epithelial–Mesenchymal Transition Through the ERK5/AP-1 Pathway</p>

Zhang

Zhao

Zhang

et al. 2020

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Background: So far, little research has been conducted regarding the underlying mechanism of renal carcinogenesis at molecular level. Epithelial-mesenchymal transition (EMT) exerts an important part during tumor genesis as well as the development through mitogen-activated protein kinase (MAPK) pathways. Therefore, we hypothesized that EMT could promote renal cell carcinoma (RCC) progression via the ERK5/AP-1pathway. Materials and Methods: The RCC cell lines were utilized to be the models with in vitro exposure to cigarette smoke extract (CSE). We used the curcumin for the EMT intervention study. In the present study, immunohistochemistry (IHC), Western blotting, and real-time quantitative reverse transcription PCR had been used to determine the experimental results. EMT phenotypic alterations were assessed by changes in cell morphology, invasion and transfer ability, as well as expression of epithelial and mesenchymal markers. Results: In human renal cell carcinoma tissue, E-cadherin expression within the smoking renal cancer patients was down-regulated compared with that among the non-smokers. However, Vimentin, N-cadherin, and TWIST levels increased (P<0.05). Significantly, we clarified that ERK5/AP-1 exerted positive regulation on the renal cell carcinoma EMT mediated by CS, which was suggested based on the results of CS activating the ERK5/AP-1 pathway, as well as ERK5 inhibition via XMD8-92 reversed AP-1 protein levels and the EMT process. Furthermore, curcumin showed the same inhibitory effect as XMD8-92 and significantly reversed CSinduced EMT through inhibiting the ERK5/AP-1 signaling pathway. Conclusion: The above results indicated that ERK5/AP-1 signaling pathway exerts a vital part for CS-associated RCC development and cancer intervention.

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