Expression Profiles of Genes—Potential Therapy Targets—and Their Relationship to Survival in Renal Cell Carcinoma

Apanovich, Natalya; Peters, M. V.; Апанович, П. В.; Камолов, Б. Ш.; Матвеев, В. Б.; Ginter, E; Карпухин, А. В.

doi:10.1134/s1607672918010040

Cited by 5 publications

(5 citation statements)

References 9 publications

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“…This subtype is notoriously resistant to traditional chemotherapy and radiotherapy (52). The primary signaling pathways underlying ccRCC pathogenesis include the PI3K/AKT and MAPK signaling pathways (53). Elevated Notch1 signaling exerts its tumor growth-promoting effects via the PI3K/AKT signaling pathway (54,55) and the oncogenic effects of specific microRNAs and the long non-coding RNA, promoter of CDKN1A antisense DNA damage activated RNA, also involve the activation of this pathway (56,57).…”

Section: Discussionmentioning

confidence: 99%

FABP5 regulates the proliferation of clear cell renal cell carcinoma cells via the PI3K/AKT signaling pathway

Wang

Zhang

et al. 2019

Int J Oncol

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Clear cell renal cell carcinoma (ccRCC) has been associated with one of the highest mortality rates among all cancers. Fatty acid binding proteins (FABPs) are 14-15 kDa proteins that are highly abundant in the cytosol of most tissues. FABP5, a member of the FABP family, has been observed to promote tumor cell growth in numerous cancer types. In order to investigate the function of FABP5 in ccRCC cells in the present study, RNA sequencing data from The Cancer Genome Atlas were analyzed to determine the expression levels of FABP5 in ccRCC patient samples. Survival and Cox regression analyses were performed to measure the association between FABP5 expression and clinicopathological features of patients with ccRCC. Subsequent in vitro experiments downregulated or overexpressed FABP5 in Caki-1 and 786O ccRCC cells using lentiviral vectors to evaluate cell proliferation ability, and a xenograft transplantation model was established to examine the effect of FABP5 on tumorigenesis in vivo. The results demonstrated that FABP5 expression was significantly upregulated in samples from patients with ccRCC when compared with normal tissue samples. High FABP5 expression was also significantly correlated with tumor and metastasis classifications and predicted poor survival in patients with ccRCC. In ccRCC cells, silencing of FABP5 significantly inhibited cell proliferation, while overexpression of FABP5 promoted cell proliferation when compared to the respective controls. In addition, treatment with the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/AKT inhibitor, LY294002, attenuated the pro-proliferative effects of exogenous FABP5 expression in Caki-1 and 786O cells. This indicated that the PI3K/AKT signaling pathway may be partially involved in the FABP5-mediated increase in ccRCC cell proliferation. Furthermore, FABP5 was observed to regulate tumor growth in nude mice in vivo. In conclusion, the results of the present study suggest that FABP5 may exert a pro-proliferative role in ccRCC and may be associated with malignant progression and tumorigenesis.

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Section: Discussionmentioning

confidence: 99%

FABP5 regulates the proliferation of clear cell renal cell carcinoma cells via the PI3K/AKT signaling pathway

Wang

Zhang

et al. 2019

Int J Oncol

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“…The principal mechanisms involved in renal carcinoma pathogenesis seem to be mediated via PI3K-AKT-mTOR, Ras-RAF-ERK, and VEGF signaling pathways, and the level of expression of the genes that are components of these pathways was positively correlated with overall survival in these patients. Therefore, further research targeting the genes and their encoded products, within these pathways, is needed to provide more insight into the involved pathways [ 92 , 93 ].…”

Section: Ckd and Malignancy—dangerous Scenarios In The Framework Omentioning

confidence: 99%

Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

Mihai

Codrici

Popescu

et al. 2018

Journal of Immunology Research

420

317

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Persistent, low-grade inflammation is now considered a hallmark feature of chronic kidney disease (CKD), being involved in the development of all-cause mortality of these patients. Although substantial improvements have been made in clinical care, CKD remains a major public health burden, affecting 10–15% of the population, and its prevalence is constantly growing. Due to its insidious nature, CKD is rarely diagnosed in early stages, and once developed, its progression is unfortunately irreversible. There are many factors that contribute to the setting of the inflammatory status in CKD, including increased production of proinflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, altered metabolism of adipose tissue, and last but not least, gut microbiota dysbiosis, an underestimated source of microinflammation. In this scenario, a huge step forward was made by the increasing progression of omics approaches, specially designed for identification of biomarkers useful for early diagnostic and follow-up. Recent omics advances could provide novel insights in deciphering the disease pathophysiology; thus, identification of circulating biomarker panels using state-of-the-art proteomic technologies could improve CKD early diagnosis, monitoring, and prognostics. This review aims to summarize the recent knowledge regarding the relationship between inflammation and CKD, highlighting the current proteomic approaches, as well as the inflammasomes and gut microbiota dysbiosis involvement in the setting of CKD, culminating with the troubling bidirectional connection between CKD and renal malignancy, raised on the background of an inflammatory condition.

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“…The PI3K/AKT/mTOR and MAPK pathway is renowned for its activity in the development of RCC [ 26 ]. Recently, studies have revealed that the release of inflammatory cytokines, such as IL-2, IL-6, IL-10, and TNF- α , and the activity of ROS which initiated RCC are modulated by the MAPK pathway [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Radix Actinidia chinensis Suppresses Renal Cell Carcinoma Progression: Network Pharmacology Prediction and In Vivo Experimental Validation

Liu

Zhang

2022

Analytical Cellular Pathology

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Background. Renal cell carcinoma (RCC) is a frequent disease with limited curative methods. This study is aimed at investigating the role and mechanism of Radix Actinidia chinensis (RAC) on RCC. Methods. The ingredients, target, and crucial pathways of RAC in RCC therapy were analyzed by network pharmacology. Then, an RCC animal model was established by subcutaneously injecting A498 cell suspension to BALB/c nude mice. After 1 week, the mice in the RAC-L/M/H groups were administered with RAC at 5, 10, and 20 mg/kg/d, respectively. The histopathology of the tumor was evaluated. The contents of tumor inflammatory cytokines and serum oxidative stress factors were detected by ELISA. The apoptosis of tumor tissues was assessed by TUNEL staining. The expressions of apoptosis-, proliferate-, autophagy-, and MAPK-related proteins were measured. Results. There were 13 active ingredients, and 20 RCC-relevant targets were selected from RAC; KEGG pathway indicated that these targets were enriched in the PI3K/AKT/mTOR and MAPK pathway. In in vivo experiments, RAC not only obviously damaged tumor cells and decreased the release of inflammatory cytokines and oxidative stress factors but also enhanced the apoptosis of the tumor cell in RCC mice. Besides, the expressions of apoptosis-, proliferate-, autophagy-, PI3K/AKT/mTOR path-, and MAPK path-related proteins were all affected by RAC. Conclusion. RAC attenuated RCC by regulating inflammation response, oxidative stress, apoptosis, proliferation, and autophagy, and its effects were partly linked to the PI3K/AKT/mTOR and MAPK pathway, which indicated that RAC may be a candidate drug for RCC.

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Expression Profiles of Genes—Potential Therapy Targets—and Their Relationship to Survival in Renal Cell Carcinoma

Cited by 5 publications

References 9 publications

FABP5 regulates the proliferation of clear cell renal cell carcinoma cells via the PI3K/AKT signaling pathway

FABP5 regulates the proliferation of clear cell renal cell carcinoma cells via the PI3K/AKT signaling pathway

Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

Radix Actinidia chinensis Suppresses Renal Cell Carcinoma Progression: Network Pharmacology Prediction and In Vivo Experimental Validation

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