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Search Results (15)
  • Open Access

    ARTICLE

    CDK4 Mediates Cisplatin Resistance in Renal Cell Carcinoma (RCC) Cells by Regulating the ASH1L-CTR1 Axis

    Wenjian Zeng1, Xianglong Li2, Hao Cai1, Qingyu Zhou2, Shuangshuang Sun2, Pingping Li2, Sunlong Li1, Zhi Chen2,*

    Oncology Research, Vol.34, No.6, 2026, DOI:10.32604/or.2026.073934 - 21 May 2026

    Abstract Objectives: Cisplatin resistance is a major obstacle in the treatment of renal cell carcinoma (RCC), severely compromising therapeutic efficacy and patient prognosis. This study aimed to clarify the role and molecular mechanism of cyclin-dependent kinase 4 (CDK4) in cisplatin resistance of RCC. Methods: Immunohistochemistry (IHC) was used to detect the expression of CDK4 in cisplatin-resistant RCC tissues. In RCC cells and their drug-resistant sublines, CDK4 overexpression/knockdown assays were performed to evaluate the effects on cisplatin resistance and malignant progression. An in vivo model was established, to verify the in vivo function of CDK4. Transcriptome sequencing (RNA-seq), Cleavage Under… More >

  • Open Access

    CASE REPORT

    Adolescent Renal Tumours: Diagnostic and Therapeutic Challenges in a Transitional Age Group—A Multidisciplinary Case Report Series from a Single Center

    Antonio Ruggiero1,2,*, Fernando Fuccillo1, Valerio Di Paola3, Alberto Romano1, Palma Maurizi1,2, Dario Talloa1, Nazario Foschi4, Pierluigi Russo4, Marco Racioppi4, Stefano Mastrangelo1,2, Giorgio Attinà1

    Oncology Research, Vol.34, No.4, 2026, DOI:10.32604/or.2026.072807 - 23 March 2026

    Abstract Background: The management of renal neoplasms in adolescent patients poses unique clinical challenges due to their transitional position between paediatric and adult populations. This age group exhibits marked heterogeneity in tumour histology, ranging from entities commonly observed in paediatric oncology to tumours typical of adult age, as well as rare histological subtypes that exceptionally affect the kidney. Given the substantial differences in clinical protocols between paediatric and adult populations, rigorous multidisciplinary evaluation is essential to determine optimal diagnostic and therapeutic strategies for adolescent patients. Case Description: We present four cases from our tertiary referral centre that… More >

  • Open Access

    ARTICLE

    Association of hypoxia-inducible factor-1α (HIF1α) 1772C/T gene polymorphism with susceptibility to renal cell carcinoma/prostate cancer

    HONGYAN LI1,#, CHUNLING LIAO2,#, WENJUAN WENG2, HONGZHEN ZHONG2, TIANBIAO ZHOU2,*

    BIOCELL, Vol.44, No.2, pp. 257-262, 2020, DOI:10.32604/biocell.2020.08826 - 27 May 2020

    Abstract In this study, we used a meta-analysis method to evaluate the relationship between hypoxia-inducible factor-1α (HIF1α) 1772C/T gene polymorphism (rs 11549465) and renal cell carcinoma (RCC)/prostate cancer risk. We searched for relevant studies (before March 1, 2019) on Cochrane Library, Embase, and PubMed. Studies meeting the inclusion criteria were recruited into this meta-analysis. The outcome of dichotomous data was showed in the way of odds ratios (OR), and 95% confidence intervals (CI) were also counted. In this investigation, there was no association between HIF1α 1772C/T gene polymorphism and susceptibility to RCC in Caucasians, Asians as More >

  • Open Access

    ARTICLE

    Kinesin Motor Protein KIFC1 Is a Target Protein of miR-338-3p and Is Associated With Poor Prognosis and Progression of Renal Cell Carcinoma

    Gang Li*, Tie Chong*, Jie Yang, Hongliang Li*, Haiwen Chen*

    Oncology Research, Vol.27, No.1, pp. 125-137, 2019, DOI:10.3727/096504018X15213115046567

    Abstract KIFC1 (kinesin family member C1) plays a critical role in clustering of extra centrosomes in various cancer cells and thus could be considered as a promising therapeutic target. However, whether KIFC1 is involved in the procession of renal cell carcinoma (RCC) still remains unclear. In this study, we found that KIFC1 was upregulated in RCC tissues and is responsible for RCC tumorigenesis (p<0.001). The high expression of KIFC1 correlates with aggressive clinicopathologic parameters. Kaplan–Meier analysis suggested that KIFC1 was associated with poor survival prognosis in RCC. Silencing KIFC1 dramatically resulted in inhibition of proliferation, delayed the More >

  • Open Access

    ARTICLE

    Knockdown of NF-κB1 by shRNA Inhibits the Growth of Renal Cell Carcinoma In Vitro and In Vivo

    Amanda Ikegami*, Luiz Felipe S. Teixeira*, Marina S. Braga, Matheus Henrique Dos S. Dias, Eduardo C. Lopes, Maria Helena Bellini*

    Oncology Research, Vol.26, No.5, pp. 743-751, 2018, DOI:10.3727/096504017X15120379906339

    Abstract Renal cell carcinoma (RCC) accounts for approximately 2%–3% of human malignancies and is the most aggressive among urologic tumors. Biological heterogeneity, drug resistance, and chemotherapy side effects are the biggest obstacles to the effective treatment of RCC. The NF-kB transcription factor is one of several molecules identified to be responsible for the aggressive phenotype of this tumor. In the past decade, several studies have demonstrated the activation of NF-kB in RCC, and many have implicated NF-kB1 (p50) as an important molecule in tumor progression and metastasis. In the present study, a lentivirus was used to… More >

  • Open Access

    ARTICLE

    MicroRNA-384 Inhibits the Growth and Invasion of Renal Cell Carcinoma Cells by Targeting Astrocyte Elevated Gene 1

    Haitao Song*, Yanwei Rao, Gang Zhang*, Xiangbo Kong*

    Oncology Research, Vol.26, No.3, pp. 457-466, 2018, DOI:10.3727/096504017X15035025554553

    Abstract MicroRNAs (miRNAs) are emerging as pivotal regulators in the development and progression of various cancers, including renal cell carcinoma (RCC). MicroRNA-384 (miR-384) has been found to be an important cancer-related miRNA in several types of cancers. However, the role of miR-384 in RCC remains unclear. In this study, we aimed to investigate the potential function of miR-384 in regulating tumorigenesis in RCC. Here we found that miR-384 was significantly downregulated in RCC tissues and cell lines. Overexpression of miR-384 significantly inhibited the growth and invasion of RCC cells, whereas inhibition of miR-384 had the opposite More >

  • Open Access

    ARTICLE

    MicroRNA-186 Suppresses Cell Proliferation and Metastasis Through Targeting Sentrin-Specific Protease 1 in Renal Cell Carcinoma

    Dan Jiao*, Man Wu, Lei Ji, Feng Liu§, Yingying Liu§

    Oncology Research, Vol.26, No.2, pp. 249-259, 2018, DOI:10.3727/096504017X14953948675430

    Abstract Recent evidence suggests that dysregulation of microRNAs is associated with the development of multiple malignancies. miR-186 has been reported as a critical cancer regulator in several types of cancers. However, its functional significance and molecular mechanism underlying renal cell carcinoma (RCC) remain unknown. In this study, our results showed that miR-186 expression was dramatically downregulated in RCC tissues and cell lines compared to that in adjacent normal tissues and cell lines. Overexpression of miR-186 significantly inhibited cell growth, colony formation, and cell invasion; caused cell cycle arrest at the G0/G1 phase; and induced cell apoptosis as… More >

  • Open Access

    ARTICLE

    Knockdown of TACC3 Inhibits the Proliferation and Invasion of Human Renal Cell Carcinoma Cells

    Feng Guo, Yaquan Liu

    Oncology Research, Vol.26, No.2, pp. 183-189, 2018, DOI:10.3727/096504017X14837020772250

    Abstract Transforming acidic coiled-coil protein 3 (TACC3) is a member of the TACC family and plays an important role in regulating cell mitosis, transcription, and tumorigenesis. However, the expression pattern and roles of TACC3 in renal cell carcinoma (RCC) remain unclear. The aim of this study was to investigate the role of TACC3 in RCC. We demonstrated overexpression of TACC3 in human RCC cell lines at both RNA and protein levels. Moreover, knockdown of TACC3 repressed RCC cell proliferation, migration, and invasion in vitro. In addition, knockdown of TACC3 inactivated PI3K/Akt signaling in RCC cells. Furthermore, More >

  • Open Access

    ARTICLE

    Tumor Protein D52 (TPD52) Inhibits Growth and Metastasis in Renal Cell Carcinoma Cells Through the PI3K/Akt Signaling Pathway

    Zhenhua Zhao1, Hui Liu1, Junqing Hou, Tieqiang Li, Xinyi Du, Xiaolei Zhao, Wenchao Xu, Weibo Xu, Junkai Chang

    Oncology Research, Vol.25, No.5, pp. 773-779, 2017, DOI:10.3727/096504016X14774889687280

    Abstract Tumor protein D52 (TPD52) is a member of the TPD52-like protein family and plays different roles in various types of malignancies. However, its role in renal cell carcinoma (RCC) is still unclear. In this study, we investigated the role of TPD52 in RCC. The mechanism of TPD52 in RCC was also investigated. Our data demonstrated that the expression levels of TPD52 in both mRNA and protein were significantly decreased in RCC cells. Overexpression of TPD52 inhibited proliferation, migration, and invasion with decreased epithelial–mesenchymal transition (EMT) phenotype in RCC cells, as well as attenuated tumor growth More >

  • Open Access

    ARTICLE

    Knockdown of Serine–Arginine Protein Kinase 1 Inhibits the Growth and Migration in Renal Cell Carcinoma Cells

    Xingtao Han*†, Jinjian Yang*, Zhankui Jia*, Pengtao Wei, Han Zhang, Wenwei Lv, Jiantao Sun, Qingxiang Huo

    Oncology Research, Vol.25, No.3, pp. 389-395, 2017, DOI:10.3727/096504016X14743324568129

    Abstract The pre-mRNA splicing regulator serine–arginine protein kinase 1 (SRPK1), a member of the SR kinase family, plays an essential role in cancer development and various pathophysiological processes. However, its expression pattern and functions in renal cell carcinoma (RCC) remain unknown. Therefore, the aim of this study was to assess the role of SRPK1 in RCC. Our data showed that SRPK1 was significantly upregulated in human RCC tissues and cell lines. SRPK1 interference significantly inhibited the proliferation of RCC cells and inhibited tumor growth in vivo. In addition, SRPK1 interference also suppressed migration and invasion in More >

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