國家衛生研究院 NHRI:Item 3990099045/9846
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    題名: The basal body gene, RPGRIP1L, is a candidate tumor suppressor gene on chromosome 16q12.2 in human hepatocellular carcinoma
    作者: Lin, YW;Yan, MD;Shih, YL
    貢獻者: National Institute of Cancer Research
    摘要: oss of heterozygosity (LOH) on chromosome 16q is one of the most frequent genetic alterations in hepatocellular carcinoma (HCC). Our previous data showed that the smallest common deleted region was between D16S415 and D16S419, encompassed approximately by a 0.75-cM region on 16q12.2 and suggested that the putative tumor suppressor genes (TSGs) at this locus might be involved in the development of HCC. Of the 4 genes (CHD9, RBL2, AKTIP and RPGRIP1L) located in this region, only RPGRIP1L was downregulated in HCCs. Downregulation of RPGRIP1L was found in 91% (10/11) HCC cell lines and 35% (14/40) HCCs, respectively. One nonsense mutation was found in one HCC and this mutation resulted in premature stop codon. To investigate the role of RPGRIP1L in HCCs, we used overexpression of RPGRIP1L in four HCC cell lines (HepG2, Huh6, Huh7, and Hep3B). Overexpression of RPGRIP1L suppressed colony formation of tumor cells. Conversely, expression of RPGRIP1LM (nonsense mutant form) in HCC cells enhanced colony formation. Furthermore, knockdown RPGRIP1L by RNA interference in SK-HepI cells promoted cell transformation. Taken together, these data strongly suggest the RPGRIP1L might be the putative TSG at chromosome 16q12.2 in HCC. Moreover, we showed that that Mad2, Survivin, and Securin were elevated in RPGRIP1LM-HepG2 transfectants and RPGRIP1L-shRNA-SK-HepI transfectants. After knockdown MAD2 in RPGRIP1L-shRNA-SK-HepI transfectants partly reverse cellular transformation capability. These data suggest that RPGRIP1L suppress cellular transformation partly through mitotic checkpoint protein Mad2.
    日期: 2009-05
    關聯: Cancer Research. 2009 May;69(9):Meeting Abstract 4950.
    Link to: http://cancerres.aacrjournals.org/content/69/9_Supplement/4450.short
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0008-5472&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000209702802291
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