Establishment and characterization of seven human renal cell carcinoma cell lines

Shin, Kihyuk; Ku, Ja Lok; Kim, W.-H.; Lee, S.-E.; Lee, C.; Kim, S.-W.; Park, J.-G.

doi:10.1046/j.1464-410x.2000.00247.x

Cited by 17 publications

(15 citation statements)

References 23 publications

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“…Here, we reported that the establishment of 10 RCC cell lines derived from human patient tumors. Only 10 of 125 patient tumors were able to be used in this regard (8.0% success rate), which is lower than that of other reports (18,19). Because of this reason, we used the nude mice to establish the RCC cell lines, and then used the SCID/beige mice to assess tumor burden and immune cell reconstitution.…”

Section: Discussionmentioning

confidence: 96%

Immunotherapy for Human Renal Cell Carcinoma by Adoptive Transfer of Autologous Transforming Growth Factor β–Insensitive CD8+ T Cells

Wang

Wen

Yuan

et al. 2010

Clinical Cancer Research

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Purpose: Transforming growth factor-β (TGF-β) is a potent immunosuppressor that has been associated with tumor evasion from the host immune surveillance and, thus, tumor progression. We tested a novel immunotherapy for human renal cell cancer (RCC) using a technique that involves the adoptive transfer of autologous tumor-reactive, TGF-β-insensitive CD8 + T cells into human RCC-challenged immunodeficient mice to identify its potent antitumor responses.Experimental Design: The present study was conducted using a one-to-one adoptive transfer strategy to treat tumor-bearing severe combined immunodeficient (SCID/beige) mouse. The SCID/beige mice were humanized with peripheral blood mononuclear cells from patients with RCC (Hu-PBMC-SCID) before adoptive transfer. Autologous CD8 + T cells were expanded ex vivo using autologous patient's dendritic cells pulsed with the tumor lysate and rendered TGF-β insensitive by dominant-negative TGF-β type II receptor. In addition, human RCC cell lines were generated using patients' tumor cells injected into SCID/beige mice. Renal cell carcinoma (RCC) is the most common solid tumor of the kidney in adults. It has previously been reported that the overproduction of TGF-β by RCC cells may lead to tumor evasion from the host immune surveillance and subsequent tumor progression (1-4). Similarly, inhibition of transforming growth factor-βTGF-β signaling using a dominant-negative TGF-β type II receptor construct (TβRIIDN) generates an immune response capable of eradicating tumors in mice challenged with live tumor cells (5).We have previously shown that murine CD8 + T cells that are rendered insensitive to TGF-β could activate the antitumor immune response cycle in prostate cancer and subsequently eradicate lung metastases (6, 7). Moreover, inhibition of TGF-β signaling in DC also enhanced the efficacy of 9). Although such TGF-β inhibition strategies are promising therapeutic approaches,

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Section: Discussionmentioning

confidence: 96%

Immunotherapy for Human Renal Cell Carcinoma by Adoptive Transfer of Autologous Transforming Growth Factor β–Insensitive CD8+ T Cells

Wang

Wen

Yuan

et al. 2010

Clinical Cancer Research

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“…A previous analysis of seven renal carcinoma cell lines also identified a genetic alteration in hMLH1. 39 Perhaps the location of hMLH1 on the short arm of chromosome 3 has biologic relevance since this region is often genetically altered in clear cell RCC. 34 Haploinsufficiency at the hMLH1 locus may be an expected and frequent event in clear cell RCC predisposing some tumor cells to MMR deficiency.…”

Section: Discussionmentioning

confidence: 99%

Mismatch Repair Gene Mutations in Renal Cell Carcinoma

Leach

Koh²,

Sharma³

et al. 2002

Cancer Biology & Therapy

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© 2 0 0 2 L a n d e s B i o s c i e n c e . N o t f o r d i s t r i b u t i o n . ABSTRACTWe investigated the spectrum and genetic basis for mismatch repair (MMR) deficiency in renal cell carcinoma (RCC) by examining expression of four MMR genes important for hereditary and sporadic carcinogenesis. MMR deficiency was assessed using microsatellite instability (MSI) and genetic analyses of 25 cell lines derived from renal tumors. MMR gene alterations were detected using reverse transcription of RNA coupled with polymerase chain reaction (RT-PCR) and DNA sequencing. Three RCC lines with undetectable MLH1 were identified and investigated for MSI and inactivating mutations in the hMLH1 MMR gene. Genetic instability and hMLH1 mutations were identified in two RCC lines and their corresponding tumors. Genetic alterations affecting expression were limited to MLH1 since other MMR proteins (MSH2, MSH6 and PMS2) were detectable in our RCC lines. Complete inactivation of MMR is apparently uncommon in RCC and occurs predominantly through inactivating mutations in the hMLH1 gene. SUMMARYMutations that completely inactivate mismatch repair gene expression are rare in RCC and occur predominantly in the hMLH1 gene located on chromosome 3. We report two cell lines with defined mutations in hMLH1 resulting in no expression and a third line with undetectable MLH1 expression or hMLH1 mutations. These RCC lines may be useful reagents for investigation of MMR dependent mechanisms of carcinogenesis and chemoresistance in localized and metastatic RCC.

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“…In particular, five cell lines were derived from clear cell RCC (SNU-228, -267, -328, -349, and -1272), one from granular RCC (SNU-482), and one from mixed clear and granular RCC (SNU-333). The mutational status of cell lines was confirmed for von Hippel-Lindau (VHL), p53, TGF-beta type II receptor (TGF-betaRII), hMSH2, and hMLH1 genes [92]. More recently, Chinese-origin cell lines named NRCC from the primary ccRCC and MRCC from the metastatic ccRCC were established from the primary tumor of a 49-year-old male ccRCC patient and the metastatic tumor of a 62-year-old male with ccRCC.…”

Section: Introductionmentioning

confidence: 99%

Choosing the right cell line for renal cell cancer research

Brodaczewska¹,

Szczylik²,

et al. 2016

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Cell lines are still a tool of choice for many fields of biomedical research, including oncology. Although cancer is a very complex disease, many discoveries have been made using monocultures of established cell lines. Therefore, the proper use of in vitro models is crucial to enhance our understanding of cancer. Therapeutics against renal cell cancer (RCC) are also screened with the use of cell lines. Multiple RCC in vitro cultures are available, allowing in vivo heterogeneity in the laboratory, but at the same time, these can be a source of errors. In this review, we tried to sum up the data on the RCC cell lines used currently. An increasing amount of data on RCC shed new light on the molecular background of the disease; however, it revealed how much still needs to be done. As new types of RCC are being distinguished, novel cell lines and the re-exploration of old ones seems to be indispensable to create effective in vitro tools for drug screening and more.Electronic supplementary materialThe online version of this article (doi:10.1186/s12943-016-0565-8) contains supplementary material, which is available to authorized users.

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Establishment and characterization of seven human renal cell carcinoma cell lines

Cited by 17 publications

References 23 publications

Immunotherapy for Human Renal Cell Carcinoma by Adoptive Transfer of Autologous Transforming Growth Factor β–Insensitive CD8+ T Cells

Immunotherapy for Human Renal Cell Carcinoma by Adoptive Transfer of Autologous Transforming Growth Factor β–Insensitive CD8+ T Cells

Mismatch Repair Gene Mutations in Renal Cell Carcinoma

Choosing the right cell line for renal cell cancer research

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