Identification of metastasis-associated proteins involved in gallbladder carcinoma metastasis by proteomic analysis and functional exploration of chloride intracellular channel 1

Wang, Jianwei; Peng, Shu-you; Li, Jiangtao; Wang, Yong; Zhang, Zhiping; Yan, CH; Cheng, De-Qing; Weng, Wei-Hong; Wu, Xiangsong; Fei, Xiaozhou; Quan, Zhiwei; Li, Jiyu; Li, Songgang; Liu, Yingbin

doi:10.1016/j.canlet.2009.02.020

Cited by 139 publications

(113 citation statements)

References 38 publications

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“…Ezrin plays a role in cell-cell interactions and cellextracellular matrix interactions by virtue of its binding to actin filaments and microtubules [40,41]. Investigations have revealed that Ezrin might be correlated with the metastasis and progression of several solid tumors, especially rhabdomyosarcoma and osteosarcoma [38,39].…”

Section: Discussionmentioning

confidence: 98%

MicroRNA-144 inhibits the proliferation, apoptosis, invasion, and migration of osteosarcoma cell line F5M2

Cui

Wang

2015

Tumor Biol.

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This study is aimed to investigate the role of microRNA-144 (miR-144) in osteosarcoma cell line F5M2 proliferation, apoptosis, invasion, and metastasis. Between 2007 and 2014, 66 cases of osteosarcoma samples in the corresponding adjacent normal tissue samples were selected from surgical resection or biopsy in the Department of Orthopedics, Shengjing Hospital, China Medical University. MiR-144 levels and Ezrin messenger RNA (mRNA) levels in osteosarcoma and the adjacent bone tissues were detected, and clinical and pathological features were analyzed. Exogenous miR-144 was transfected into human osteosarcoma cell lines at two different concentrations (low and high), and the expression levels of miR-144 and Ezrin protein between highly metastatic osteosarcoma cells and lowly metastatic osteosarcoma cells were compared. Real-time polymerase chain reaction (RT-PCR) and Western blot were used for detecting the expression levels of miR-144 or Ezrin protein, respectively. Cell proliferation was measured by methylthiazol tetrazolium (MTT) assay. Cell invasion and migration was evaluated by Transwell assays. Finally, flow cytometry was employed to determine the cell apoptosis. MiR-144 expression in osteosarcoma tissue was significantly lower than that in the surrounding normal bone tissue (P < 0.001), while Ezrin mRNA expression in osteosarcoma tissue was significantly higher than that in the surrounding normal bone tissue (P < 0.001); correlation analysis showed a significant negative correlation between miR-144 and Ezrin mRNA levels (r = 0.982, P < 0.001). MiR-144 and Ezrin mRNA expressions were significantly related with cell metastasis (P < 0.05) but were not related with other clinical factors such as gender, age, tumor location, tumor size, Enneking staging, and Dahlin's histological classification. The results of RT-PCR showed that the expression level of miR-144 in osteosarcoma cells increased after transfected with exogenous miR-144 mimics, and this increase positively correlated with the transfection concentration of miR-144 mimics. Furthermore, Western blotting revealed a significant and dose-dependent decrease in Ezrin protein levels in F5M2 cells transfected with miR-144. MTT and Transwell assays showed that the invasion and metastasis of F5M2 cells was significantly decreased following exogenous overexpression of miR-144. Our study supports the view that the miR-144 may regulate Ezrin protein expression by inhibiting the invasion and metastasis of osteosarcoma cells.

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Section: Discussionmentioning

confidence: 98%

MicroRNA-144 inhibits the proliferation, apoptosis, invasion, and migration of osteosarcoma cell line F5M2

Cui

Wang

2015

Tumor Biol.

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“…[1][2][3][4][5][6][7][8][9] Curative resection is the only cure for this highly lethal malignancy. However, owing to its non-specific symptoms and highly invasive nature, most patients are at an advanced stage when they are diagnosed.…”

Section: Introductionmentioning

confidence: 99%

MALAT1 promotes the proliferation and metastasis of gallbladder cancer cells by activating the ERK/MAPK pathway

Wang

et al. 2014

Cancer Biology & Therapy

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“…DISCUSSION GBC represents the most common and aggressive carcinoma of biliary tract. Up to now, surgical resection is still considered the curative treatment option (13,14). Unfortunately, most GBC are diagnosed at advanced stages with the unresectable tumor, leading to a poor survival outcome (15,16).…”

Section: Fig 3 Effects Ofep Administration On Gbc Cell Independent mentioning

confidence: 99%

Ethyl Pyruvate Administration Suppresses Growth and Invasion of Gallbladder Cancer Cells via Downregulation of Hmgb1-Rage Axis

et al. 2012

Int J Immunopathol Pharmacol

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The first two authors contributed equally to this work High mobility group box Bl (HMGBl)-receptor for advanced glycation endproducts (RAGE) axis has been previously known to be involved in carcinogenesis and development of multiple malignancies. Some studies have confirmed that Ethyl pyruvate (EP), a potent inhibitor of HMGBl, exerts the therapeutic effects on metastatic live tumor from gastric cancer. However, the effects and possible molecular mechanisms of EP on gallbladder cancer (GBC) need to be further explored. In the present study, human GBC cell lines (GBC-SD and SGC-996) were treated with different concentrations of EP. Then, the expression levels of HMGBl, RAGE and some transcription factors were identified by Real-time PCR and Western blot assays. Cell proliferative activities indicated by MTT assay, invasive potential by Transwell assay and cell apoptosis and cycle distribution were performed for functional analysis of GBC cell lines in vitro. As a result, EP decreased the expression of HMGBll, RAGE, PCNA and matrix metallopeptidase-9 (MMP-9), while it increased the expression of p53. Moreover, EP administration decreased GBC cell proliferation, inhibited the invasive potential, and induced apoptosis and cycle arrest in S phase in GBC cells. In conclusion, EP administration inhibits growth and invasion of gallbladder cancer cells possibly via down-regulation of the HMGBl-RAGE axis, suggesting that EP may playa critical role in the treatment of cancer in conjunction with other therapeutic agents.High mobility group BI (HMGBI) has been known for its intracellular function as the intranuclear non-histone DNA binding protein and is regarded as an essential position in DNA repair. HMGBI and its counter-receptor, receptor for advanced glycation endproducts (RAGE), represent suitable targets for investigation, integrating many aspects of modem biology, particularly that associated with cancer (1). Originally, amphoterin, the major production of HMGB1, is over-expressed and closely associated with tumor invasion and metastasis. In human dendritic cells, RAGE is required for the effect of HMGB1 on cell expansion and survival. HMGB1/ RAGE interaction results in downstream activation of MAPK and NF-KB, representing a profitable evolutionary mechanism (2). Over-expression of HMGBI/RAGE, especially with membranous pattern, is associated with malignant potential

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Identification of metastasis-associated proteins involved in gallbladder carcinoma metastasis by proteomic analysis and functional exploration of chloride intracellular channel 1

Cited by 139 publications

References 38 publications

MicroRNA-144 inhibits the proliferation, apoptosis, invasion, and migration of osteosarcoma cell line F5M2

MicroRNA-144 inhibits the proliferation, apoptosis, invasion, and migration of osteosarcoma cell line F5M2

MALAT1 promotes the proliferation and metastasis of gallbladder cancer cells by activating the ERK/MAPK pathway

Ethyl Pyruvate Administration Suppresses Growth and Invasion of Gallbladder Cancer Cells via Downregulation of Hmgb1-Rage Axis

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