Yes-associated protein 1 (YAP1) promotes human gallbladder tumor growth via activation of the AXL/MAPK pathway

Li, Maolan; Lu, Jianhua; Zhang, Fei; Li, Huaifeng; Zhang, Bingtai; Wu, Xiangsong; Tan, Zhen; Zhang, Lin; Gao, Guofeng; Mu, Jian; Shu, Yijun; Bao, Runfa; Ding, Qichen; Wu, Wenzhi; Dong, Ping; Gu, Jun; Liu, Yingbin

doi:10.1016/j.canlet.2014.08.036

Cited by 61 publications

(57 citation statements)

References 29 publications

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“…The molecular classification of gallbladder cancer has identified a number of protein-coding genes as valuable biomarkers and prognostic indicators (4,5,23). However, a poor overlap exists between these biomarkers of gallbladder cancer.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA GCASPC, a Target of miR-17-3p, Negatively Regulates Pyruvate Carboxylase–Dependent Cell Proliferation in Gallbladder Cancer

et al. 2016

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Long noncoding RNAs (lncRNA) are being implicated in the development of many cancers. Here, we report the discovery of a critical role for the lncRNA GCASPC in determining the progression of gallbladder cancer. Differentially expressed lncRNAs and mRNAs between gallbladder cancer specimens and paired adjacent nontumor tissues from five patients were identified and validated by an expression microarray analysis. Quantitative real-time PCR was used to measure GCASPC levels in tissues from 42 gallbladder cancer patients, and levels of GCASPC were confirmed further in a separate cohort of 89 gallbladder cancer patients. GCASPC was overexpressed or silenced in several gallbladder cancer cell lines where molecular and biological analyses were performed. GCASPC levels were significantly lower in gallbladder cancer than adjacent nontumor tissues and were associated with tumor size, American Joint Committee on Cancer tumor stage, and patient outcomes. GCASPC overexpression suppressed cell proliferation in vitro and in vivo, whereas GCASPC silencing had opposite effects. By RNA pull-down and mass spectrometry, we identified pyruvate carboxylase as an RNAbinding protein that associated with GCASPC. Because GCASPC is a target of miR-17-3p, we confirmed that both miR-17-3p and GCASPC downregulated pyruvate carboxylase level and activity by limiting protein stability. Taken together, our results defined a novel mechanism of lncRNA-regulated cell proliferation in gallbladder cancer, illuminating a new basis for understanding its pathogenicity. Cancer Res; 76(18); 5361-71. Ó2016 AACR.

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Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA GCASPC, a Target of miR-17-3p, Negatively Regulates Pyruvate Carboxylase–Dependent Cell Proliferation in Gallbladder Cancer

et al. 2016

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“…The deregulation of cell cycle progression is a hallmark of tumor growth [24,25]. To determine whether japonicone A inhibited cell cycle progression, cell cycle distribution and related regulators were studied.…”

Section: Japonicone a Induces G0/g1 Arrest In H441 And H520 Cellsmentioning

confidence: 99%

Japonicone A inhibits the growth of non-small cell lung cancer cells via mitochondria-mediated pathways

Gong

Tian

et al. 2015

Tumor Biol.

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Japonicone A, which is a natural product isolated from the aerial part of Inula japonica Thunb., has a wide range of clinical applications, including anti-inflammation and anti-oxidation. This study investigated the effects of japonicone A on the growth of non-small cell lung cancer (NSCLC) cell lines. The results showed that japonicone A significantly inhibited the growth of NSCLC cell lines in a dose- and time-dependent manner. This product also blocked cell cycle progression at S phase and induced mitochondrial-related apoptosis by upregulating Bax, cleaved caspase-9, cleaved caspase-3, and cleaved poly(ADP-ribose) polymerase (PARP) protein levels and by downregulating Bcl-2, cyclin D1, CDC25A, and CDK2 protein levels. In vivo, japonicone A suppressed tumor growth via the same mechanism as that observed in vitro. In conclusion, our study is the first to report that japonicone A has an inhibitory effect on the growth of NSCLC cells, indicating that japonicone A administration is a potential therapeutic approach for future NSCLC treatments.

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“…Mouse KO: various cancer types developed [141] TSG: downregulation in CRC [142] TAZ Mutations in Barth syndrome [143] OG: overexpression in breast cancer [144], HCC [145] OG: overexpression in CRC [85] YAP1 OG: overexpression in NSCLC [88], prostate [90], breast [91], gallbladder cancer [146] and glioma [89] TSG: decreased expression in breast cancer [92] OG: overexpression in CRC [83], in CRC cases resistant to cetuximab [102] TSG: underexpression in CRC [79] AML -acute myeloid leukaemia; CCL -cancer cell line(s); HCC -hepatocellular carcinoma; KO -knock out; LOH -loss of heterozygosity; NSCLC -non-small cell lung cancer; OG -oncogene; TSG -tumour suppressor gene epinephrine or glucagon repress YAP1/TAZ activity [45,46]. YAP1 could also be regulated by matrix stiffness independently from LATS1/2 phosphorylation.…”

Section: Mob1 Mob1mentioning

confidence: 99%

The Hippo pathway in colorectal cancer

Wierzbicki

Rybarczyk

2015

Folia Histochem Cytobiol.

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Colorectal cancer (CRC) is one the most frequently diagnosed neoplastic diseases worldwide. Currently, aside from traditional chemotherapy, advanced CRCs are treated with modern drugs targeting cellular components such as epithelial growth factor receptor (EGFR). Since up to 70% of metastasized CRCs are drug resistant, the description of recent progress in cellular homeostasis regulation may shed new light on the development of new molecular targets in cancer treatment. The Hippo pathway has recently become subject of intense investigations since it plays a crucial role in cell proliferation, differentiation, apoptosis and tumourigenesis. Components of the Hippo pathway are deregulated in various human malignancies, and expression levels of its major signal transducers were proposed as prognostic factors in colorectal cancer. In this review we focused on recent data regarding Hippo pathway, its up-stream signals and down-stream effectors. Hippo negatively regulates its major effectors, YAP1 and TAZ kinases, which act as transcriptional co-activators inducing expression of genes involved not only in tissue repair and proliferation but are also oncoproteins involved in tumour development and progression. The deregulation of Hippo pathway components was found in many malignancies. The interactions between Hippo and Wnt/b-catenin signalling, crucial in the maintenance of cell homeostasis, have been described in relation to the control of intestinal stem cell proliferation and CRC development. The recently discovered positive feedback loop between activated YAP1 and increased EGFR/KRAS signalling found in oesophageal, ovarian and hepatocellular cancer has been related to the CRC progression and resistance to EGFR inhibitors during CRC therapy.

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Yes-associated protein 1 (YAP1) promotes human gallbladder tumor growth via activation of the AXL/MAPK pathway

Cited by 61 publications

References 29 publications

Long Noncoding RNA GCASPC, a Target of miR-17-3p, Negatively Regulates Pyruvate Carboxylase–Dependent Cell Proliferation in Gallbladder Cancer

Long Noncoding RNA GCASPC, a Target of miR-17-3p, Negatively Regulates Pyruvate Carboxylase–Dependent Cell Proliferation in Gallbladder Cancer

Japonicone A inhibits the growth of non-small cell lung cancer cells via mitochondria-mediated pathways

The Hippo pathway in colorectal cancer

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