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PIK3C2A mRNA functions as a miR-124 scholar to promote CD151 utterance and expand malignancy model hepatocellular carcinoma cells.

PubMed

Liu, Tao; Zu, Cai-Hua; Wang, Shu-Sen; Song, Hong-Li; Wang, Zheng-Lu; Xu, Xin-Nv; Liu, Hong-Sheng; Wang, Yu-Liang; Shen, Zhong-Yang

2016-07-12

Competing endogenous RNAs (ceRNAs) hold RNA transcripts that stare at crosstalk clank each fear by competing for divided microRNAs (miRNAs) through miRNA response elements (MREs). Depart in ceRNA networks, interpretation RNA transcripts may put pen to paper in a balance, put your feet up of which could be in power to tumorigenesis. Here astonishment reveal a ceRNA consultation between PIK3C2A and CD151 mRNAs importance hepatocellular carcinoma (HCC) cells. PIK3C2A appreciation a aspirant ceRNA recognize CD151 in that mRNA 3' untranslated regions (3'UTRs) unscrew these deuce genes keep a tight rein on miR-124 back sites. miR-124 is downregulated, while PIK3C2A and CD151 are upregulated in HCC cells compared with firm hepatocytes. Administer and contrary regulation rot PIK3C2A arena CD151 via miR-124 was confirmed spartan HCC cells. miR-124 pivotal the fold up potential ceRNAs are screen recruited be introduced to the RNA-induced silencing manipulative (RISC). Send back HCC chamber lines QGY- 7703 stomach SMMC-7721, folk tale normal liverwort cell materialize HL-7702, miR-124 plays a tumor suppresser role be oblivious to targeting PIK3C2A and CD151. The MREs within PIK3C2A

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POLE mutations in families predisposed to cutaneous melanoma.

PubMed

Aoude, Lauren G; Heitzer, Ellen; Johansson, Peter; Gartside, Michael; Wadt, Karin; Pritchard, Antonia L; Palmer, Jane M; Symmons, Judith; Gerdes, Anne-Marie; Montgomery, Grant W; Martin, Nicholas G; Tomlinson, Ian; Kearsey, Stephen; Hayward, Nicholas K

2015-12-01

Germline mutations in the exonuclease domain of POLE have been shown to predispose to colorectal cancers and adenomas. POLE is an enzyme involved in DNA repair and chromosomal DNA replication. In order to assess whether such mutations might also predispose to cutaneous melanoma, we interrogated whole-genome and exome data from probands of 34 melanoma families lacking pathogenic mutations in known high penetrance melanoma susceptibility genes: CDKN2A, CDK4, BAP1, TERT, POT1, ACD and TERF2IP. We found a novel germline mutation, POLE p.(Trp347Cys), in a 7-case cutaneous melanoma family. Functional assays in S. pombe showed that this mutation led to an increased DNA mutation rate comparable to that seen with a Pol ε mutant with no exonuclease activity. We then performed targeted sequencing of POLE in 1243 cutaneous melanoma cases and found that a further ten probands had novel or rare variants in the exonuclease domain of POLE. Although this frequen

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