<scp>STAT</scp>s profiling reveals predominantly‐activated <scp>STAT3</scp> in cholangiocarcinoma genesis and progression

Dokduang, Hasaya; Techasen, Anchalee; Namwat, Nisana; Khuntikeo, Narong; Pairojkul, Chawalit; Murakami, Yoshinori; Loilome, Watcharin; Yongvanit, Puangrat

doi:10.1002/jhbp.131

Cited by 42 publications

(39 citation statements)

References 49 publications

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“…Since the proteins affected by metformin treatment, as observed in this study, can be mediated by NF-ĸB and STAT3, important transcription factors in carcinogenesis and progression of CCA (15,16), it was thus interesting to investigate whether metformin affected CCA cells via NF-ĸB or STAT3 pathways. The levels of NF-ĸB (p65) and STAT3 from whole-cell lysates of CCA cells treated with 10 and 20 mM metformin for 48 h and the control cells were determined using western blots.…”

Section: Metformin Inhibited Nuclear Localization Of Nf-ĸb and Stat3 mentioning

confidence: 89%

“…To investigate the alternative pathways in response to metformin treatment, NF-ĸB and STAT3, the major transcription factors reported in development and progression of liver fluke-associated CCA (15,16) were further examined. The results from western blots of whole-cell lysates showed no differences of p-STAT3 at both Y705 and S727 and the expression levels of p65 between the controls and the metformin-treated cells.…”

Section: Discussionmentioning

confidence: 99%

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Metformin Exerts Antiproliferative and Anti-metastatic Effects Against Cholangiocarcinoma Cells by Targeting STAT3 and NF-ĸB

Saengboonmee

Seubwai

Cha’on

et al. 2017

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Section: Metformin Inhibited Nuclear Localization Of Nf-ĸb and Stat3 mentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Metformin Exerts Antiproliferative and Anti-metastatic Effects Against Cholangiocarcinoma Cells by Targeting STAT3 and NF-ĸB

Saengboonmee

Seubwai

Cha’on

et al. 2017

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“…Several studies has indicated that CCA is caused by dysregulation of the tumor suppressor genes or oncogenes (Loilome et al, 2011;Namwat et al, 2012;Dokduang et al, 2014) However, the molecular mechanism(s) for CCA carcinogenesis remains unclear. Several studies have demonstrated that alteration of PI3K/AKT/PTEN and Wnt/ β-catenin was found in many cancers and these pathways may serve as the potential targets for cancer treatment (Gong et al, 2012;Pandurangan, 2013;Jannesari-Ladani et al, 2014;Tan et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Opisthorchis viverrini Infection Activates the PI3K/AKT/PTEN and Wnt/β-catenin Signaling Pathways in a Cholangiocarcinogenesis Model

Yothaisong¹,

Thanee²,

Namwat³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Opisthorchis viverrini (Ov) infection is the major etiological factor for cholangiocarcinoma (CCA), especially in northeast Thailand. We have previously reported significant involvement of PI3K/AKT/PTEN and Wnt/β-catenin in human CCA tissues. The present study, therefore, examined the expression and activation of PI3K/ AKT/PTEN and Wnt/β-catenin signaling components during Ov-induced cholangiocarcinogenesis in a hamster animal model. Hamsters were divided into two groups; non-treated and Ov plus NDMA treated. The results of immunohistochemical staining showed an upregulation of PI3K/AKT signaling as determined by elevated expression of the p85α-regulatory and p110α-catalytic subunits of PI3K as well as increased expression and activation of AKT during cholangiocarcinogenesis. Interestingly, the staining intensity of activated AKT (p-AKT) increased in the apical regions of the bile ducts and strong staining was detected where the liver fluke resides. Moreover, PTEN, a negative regulator of PI3K/AKT, was suppressed by decreased expression and increased phosphorylation during cholangiocarcinogenesis. We also detected upregulation of Wnt/β-catenin signaling as determined by increased positive staining of Wnt3, Wnt3a, Wnt5a, Wnt7b and β-catenin, corresponded with the period of cholangiocarcinogenesis. Furthermore, nuclear staining of β-catenin was observed in CCA tissues. Our results suggest the liver fluke infection causes chronic inflammatory conditions which lead to upregulation of the PI3K/AKT and Wnt/β-catenin signaling pathways which may drive CCA carcinogenesis. These results provide useful information for drug development, prevention and treatment of CCA.

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“…STAT3 plays important roles in the inflammation that contributes to carcinoma [36]. TAMs can decrease antigen presenting ability and promote the proliferation and growth of tumor cells [37].…”

Section: Tams and Breast Cancermentioning

confidence: 99%

Tumor-associated macrophages in cancers

Zhang

et al. 2015

Clin Transl Oncol

115

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Tumor-associated macrophages (TAMs) are major component of leukocytic infiltrate of tumors and play important roles in progression and regression of tumors. Tumor microenvironment determines the mutual conversion between M1 and M2 macrophages. In many kinds of tumors, M2 type macrophages are of the majority in TAMs and promote tumor progression and metastasis. The dynamic balance and interaction between TAMs and tumor cells have important effects on the occurrence and development of tumor. TAMs in malignant tumors are useful for clinical diagnosis and may provide a novel target for cancer treatment.

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STATs profiling reveals predominantly‐activated STAT3 in cholangiocarcinoma genesis and progression

Abstract: STAT3 is the major STAT, which plays roles in the inflammation that contributes to CCA carcinogenesis and progression and may serve as a marker for a poor prognosis of CCA.

Cited by 42 publications

References 49 publications

Metformin Exerts Antiproliferative and Anti-metastatic Effects Against Cholangiocarcinoma Cells by Targeting STAT3 and NF-ĸB

Metformin Exerts Antiproliferative and Anti-metastatic Effects Against Cholangiocarcinoma Cells by Targeting STAT3 and NF-ĸB

Opisthorchis viverrini Infection Activates the PI3K/AKT/PTEN and Wnt/β-catenin Signaling Pathways in a Cholangiocarcinogenesis Model

Tumor-associated macrophages in cancers

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