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Abstract. Background/Aim: Due to its poor prognosis, it is increasingly necessary to understand the biology of renal cell cancer (RCC). Therefore, we investigated the role of microRNAs miR-1 and miR-21 in the growth of RCC cells compared to that of non-malignant renal cells. Materials and Methods: Four malignant cell lines RCC4, A498) Tumorigenesis gives cells an advantage in survival by an increase of proliferation, angiogenesis, immunomodulation and immortality (1-4). Due to its delayed diagnosis until advanced stages, renal cell cancer (RCC) is known as the deadliest neoplasm of the urinary tract (1, 5). Thus, it is more necessary than ever to understand its tumor biology and explore new targets for further therapeutic approaches and prognostic options (6). Former studies suggested that among others, a misguided microRNA expression pattern may be involved in tumor initiation and progression in RCC (7,8). Among such mechanisms, small regulatory RNAs, so-called microRNAs (miRs), can operate as controllers of different proccesses in tumorigenesis, such as cell migration and differentiation, as well as metastasis and apoptosis (9-11). miR-1 and miR-21 are two of numerous representatives of microRNAs. miR-1, initially found in cardiac muscle cells (12), but also found in various tissues (13-15), was strongly suspected of acting as a tumor suppressor due to its antioncogenic properties (16) in prostate, breast and colorectal cancer (13-15); interestingly, the type of tissue in fact determines the biological behavior of miR-1 (9). Sadly, the current data situation for the expression of miR-1 in RCC leaves much to be desired. For this reason, our study aimed to expand the first findings in order to gain a better understanding of the tumor biology of RCC. Similarly to miR-1, miR-21 was also detected in various malignant tissues, such as prostate and lung cancer and their metastases, pancreatic cancer and colorectal cancer (17-21). However, in contrast to miR-1, miR-21 appears to be an oncomir. There are preliminary investigations, showing miR-21 to appear as an oncomir in the case of RCC (22, 23).The fact that cancer cells have a further survival advantage by extending their chromosomal ends by means of endogenic telomerase, not only raises a problem, but also provides a therapeutic approach in cancer therapy (4).In order to gain deeper insight into these issues, as far as we are aware, we are the first to investigate one non-malignant 625 This article is freely accessible online. *These Authors contributed equally to this study. Materials and MethodsCell culture. Human RCC cell lines Caki-1, 786-O, A498 (all Cell Lines Service, Eppelheim, Germany), and RCC4 (Sigma-Aldrich, München, Germany) and the non-malignant renal cell line RC-124 (Cell Lines Service) were applied in this study. Caki-1 and A498 cells were propagated in minimum essential medium (MEM) supplemented with 79.6 mg/l non-essential amino acids, 2 mM L-glutamine, 1 mM sodium pyruvate, 1% penicillline/streptomycin (P/S), and 10% fetal bovine serum (FBS...

Objective Cytokines and chemokines are widely involved in cancer cell progression and thus represent promising candidate factors for new biomarkers. Methods Four renal cell cancer (RCC) cell lines (Caki-1, 786-O, RCC4, and A498) and a nonmalignant renal cell line (RC-124) were examined with respect to their proliferation. The cytokine and chemokine expression pattern was examined by a DNA array (Human Cytokines & Chemokines RT2 Profiler PCR Array; Qiagen, Hilden, Germany), and expression profiles were compared. Results Caki-1 and 786-O cells exhibited significantly increased proliferation rates, whereas RCC4 and A498 cells demonstrated attenuated proliferation, compared to nonmalignant RC-124 cells. Expression analysis revealed 52 cytokines and chemokines primarily involved in proliferation and inflammation and differentially expressed not only in malignant and nonmalignant renal cells but also in the four RCC cell lines. Conclusion This is the first study examining the expression of 84 cytokines and chemokines in four RCC cell lines compared to that in a nonmalignant renal cell line. VEGFA, NODAL, and BMP6 correlated with RCC cell line proliferation and, thus, may represent putative clinical biomarkers for RCC progression as well as for RCC diagnosis and prognosis.

Introduction: Inhibition of androgen synthesis by abiraterone acetate (AA) entails enhanced overall survival rates and clinical benefit for patients with locally advanced and metastasized prostate cancer (PC). The expression of heat shock protein 27 (HSP27) is generally associated with cytoprotection and was demonstrated to mediate chemoresistance under cytostatic therapy, for instance, docetaxel treatment. In this study, we investigated the impact of AA treatment on HSP27 expression and PC cell growth. Materials and Methods: HSP27 expression levels in docetaxel and AA-treated PC cell lines LNCaP and PC-3 were determined by SDS PAGE and Western blot analysis. Proliferation assays were performed using a CASY Cell Counter and Analyzer Model TT (Roche Applied Science). Results: Despite significantly increased HSP27 expression in PC cells incubated with docetaxel, Western blot analysis implicated a significant reduction of the cytoprotective HSP27 in AA-treated PC cells. Notably, HSP27 stably overexpressed in PC-3-HSP27 cells did not appear as an HSP27-mediated proliferation benefit in the presence of AA as shown in docetaxel incubation studies. Conclusion: In contrast to repeatedly demonstrated HSP27-driven chemoresistance related to chemotherapeutics, our results may constitute a broader molecular mode of action of AA chemotherapy. AA efficacy may exert an HSP27 suppressive role that goes beyond the primarily assumed inhibition of androgen biosynthesis.