LASP-1 induces proliferation, metastasis and cell cycle arrest at the G2/M phase in gallbladder cancer by down-regulating S100P via the PI3K/AKT pathway

Li, Zhizhen; Chen, Yuanyuan; Wang, Xuan; Zhang, HongChen; Zhang, Yijian; Gao, Yaohui; Weng, Mingzhe; Wang, Lei; Liang, Haibin; Li, MaoLan; Zhang, Fei; Zhao, Shuai; Liu, Shibo; Yang, Cao; Shu, Yijun; Bao, Runfa; Zhou, Jian; Liu, Xiyong; Yan, Yun; Lei, Zhen; Dong, Qian; Liu, Yingbin

doi:10.1016/j.canlet.2016.01.008

Cited by 44 publications

(54 citation statements)

References 24 publications

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“…Additionally, our data suggest that the expression of S100Pis positively correlated with LPXN expression in bladder cancer tissues and cells viaPI3K/AKT pathway. Our results are further supported by Li and colleagues [23], who observed that the expression of LASP-1, a focal adhesion adaptor protein, was closely related with S100P expression in gallbladder cancer. It was therefore suggested that LASP-1 might play a significant role in regulating metastasis of gallbladder cancer by down-regulating S100P via the PI3K/AKT pathway.…”

Section: Discussionsupporting

confidence: 80%

Leupaxin Promotes Bladder Cancer Proliferation, Metastasis, and Angiogenesis Through the PI3K/AKT Pathway

Hou

Zhou

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Leupaxin (LPXN) is a member of the paxillin protein family. Several studies have reported that LPXN regulates cancer development; however, the role of LPXN in bladder cancer remains unknown. Methods: The expression of LPXN in bladder cancer cells and tissues was determined by real-time PCR, western blotting, and immunohistochemistry, respectively. The biological role of LPXN in bladder cancer cell proliferation, invasion, and angiogenesis was explored both in vitro and in vivo. Results: LPXN expression was elevated in bladder cancer tissues and cell lines compared to adjacent non-tumor tissues and normal urothelial cells. High LPXN expression was correlated with large tumor size, advanced tumor stage, and poor survival in bladder cancer patients. Overexpression of LPXN significantly promoted the proliferation, invasion, and angiogenesis of bladder cancer cells, while suppressing LPXN had the opposite effects. The impact on tumor progression was abolished by inhibiting PI3K/ AKT signaling pathway. We further demonstrated that LPXN probably up-regulated S100P via the PI3K/AKT pathway. Conclusions: LPXN may facilitate bladder cancer progression by upregulating the expression of S100P via PI3K/AKT pathway. These results provide a novel insight into the role of LPXN in tumorigenesis and progression of bladder cancer and potential therapeutic target of bladder cancer.

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Section: Discussionsupporting

confidence: 80%

Leupaxin Promotes Bladder Cancer Proliferation, Metastasis, and Angiogenesis Through the PI3K/AKT Pathway

Hou

Zhou

Wang

et al. 2018

Cell Physiol Biochem

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“…Various mechanisms have been suggested to contribute to the progression of gallbladder cancer, in particular mutations in components of cell cycle or apoptotic pathways, and the processes of signal transduction, angiogenesis, invasion, and metastasis [21–23]. Apoptosis signaling cascades can be divided into 2 major pathways: a death-receptor-induced extrinsic pathway and a mitochondria-apoptosome-mediated intrinsic pathway [24].…”

Section: Resultsmentioning

confidence: 99%

Casticin induces apoptosis and G0/G1 cell cycle arrest in gallbladder cancer cells

et al. 2017

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BackgroundCasticin, the flavonoid extracted from Vitex rotundifolia L, exerts various biological effects, including anti-inflammatory and anti-cancer activity. The aim of this study is to investigate the effects and mechanisms of casticin in human gallbladder cancer cells.MethodsHuman NOZ and SGC996 cells were used to perform the experiments. CCK-8 assay and colony formation assay were performed to evaluate cell viability. Cell cycle analyses and annexin V/PI staining assay for apoptosis were measured using flow cytometry. Western blot analysis was used to evaluate the changes in protein expression, and the effect of casticin treatment in vivo was experimented with xenografted tumors.ResultsIn this study, we found that casticin significantly inhibited gallbladder cancer cell proliferation in a dose- and time-dependent manner. Casticin also induced G0/G1 arrest and mitochondrial-related apoptosis by upregulating Bax, cleaved caspase-3, cleaved caspase-9 and cleaved poly ADP-ribose polymerase expression, and by downregulating Bcl-2 expression. Moreover, casticin induced cycle arrest and apoptosis by upregulating p27 and downregulating cyclinD1/cyclin-dependent kinase4 and phosphorylated protein kinase B. In vivo, casticin inhibited tumor growth.ConclusionCasticin induces G0/G1 arrest and apoptosis in gallbladder cancer, suggesting that casticin might represent a novel and effective agent against gallbladder cancer.

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“…The TRIM32 antibody (Proteintech Group) served as the primary antibody. Scoring was conducted as described previously 16. The proportion of the immunopositive area was scored (0, 0% cells; 1, <5% cells; 2, 5%‐50% cells; 3, >50% cells), and the intensity of expression was determined (0, none; 1, low; 2, intermediate; 3, strong).…”

Section: Methodsmentioning

confidence: 99%

TRIM32 promotes cell proliferation and invasion by activating β‐catenin signalling in gastric cancer

Wang

et al. 2018

J Cellular Molecular Medi

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The tripartite motif (TRIM) family comprises more than 70 members involved in the regulation of many cellular pathways. TRIM32 acts as an E3 ubiquitin ligase and has been reported to participate in many human cancers. Here, we aimed to investigate the role of TRIM32 in gastric cancer (GC) and the clinical implications. High expression of TRIM32 was observed in GC tissues and cell lines, and was significantly associated with poor prognosis. Knockdown TRIM32 expression remarkably suppressed the proliferation, migration, and invasion of GC cells in vitro and tumour growth in vivo, whereas overexpression of TRIM32 yielded the opposite results. Western blotting and quantitative reverse‐transcription PCR (qRT‐PCR) analyses revealed that up‐regulation of TRIM32 significantly enhanced expression of β‐catenin protein and of its downstream targets TCF1, cyclin D1, Axin2 and MMP7 mRNAs. Moreover, we found that the mechanism behind the TRIM32‐promoted GC progression was related to the β‐catenin signalling pathway. Collectively, these data suggest that TRIM32 promotes GC cell proliferation, migration, and invasion by activating the β‐catenin signalling pathway.

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LASP-1 induces proliferation, metastasis and cell cycle arrest at the G2/M phase in gallbladder cancer by down-regulating S100P via the PI3K/AKT pathway

Cited by 44 publications

References 24 publications

Leupaxin Promotes Bladder Cancer Proliferation, Metastasis, and Angiogenesis Through the PI3K/AKT Pathway

Leupaxin Promotes Bladder Cancer Proliferation, Metastasis, and Angiogenesis Through the PI3K/AKT Pathway

Casticin induces apoptosis and G0/G1 cell cycle arrest in gallbladder cancer cells

TRIM32 promotes cell proliferation and invasion by activating β‐catenin signalling in gastric cancer

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