Prognostic value of phosphorylated STAT3 in advanced rectal cancer: a study from 104 French patients included in the EORTC 22921 trial

Monnien, Franck; Zaki, H. Mahamadou; Borg, Christophe; Mougin, Christiane; Bosset, Jean-François; Mercier, Mariette; Arbez-Gindre, Francine; Kantélip, B.

doi:10.1136/jcp.2010.076414

Cited by 28 publications

(35 citation statements)

References 45 publications

(30 reference statements)

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“…The Stat3 activation is transient and tightly controlled in normal cells [24][25][26][27]. On the contrary, the constitutively activated Stat3 protein has been found to be in leukemia, melanoma, cancers of the breast, head and neck, prostate, and pancreas [28,29]. Interestingly, except its role in oncogenesis, such activated Stat3 protein are associated with metastases of thymic epithelial tumors, colorectal adenocarcinoma, and cutaneous squamous cell carcinoma, and renal cell carcinoma [30][31][32].…”

Section: Discussionmentioning

confidence: 99%

Stat3 promotes invasion of esophageal squamous cell carcinoma through up-regulation of MMP2

Xuan

Lou

et al. 2014

Mol Biol Rep

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Stat3 alters the expression of its downstream genes and is associated with tumor invasion and metastasis in several human cancers. Its role in esophageal squamous cell carcinoma (ESCC) has not been well characterized. We examined the tumor sections of 100 cases of ESCC by immunohistochemistry and observed significant overexpression of Stat3 in the cytoplasm of 89% of ESCC cells and of phosphorylated Stat3 (p-Stat3) in the nuclei of 71% of ESCC when compare with normal esophageal mucosa (72%, p = 0.02; and 31%, p = 0.001). Overexpression of Stat3 and p-Stat3 positively correlated with that of matrix metalloproteinase-2 (MMP2), a known regulator for cell migration, in 65% of ESCC while only 26% shown in benign esophageal mucosa. To further investigate the association of Stat3 with tumor metastasis in vitro, invasion of EC-1 cells (a human ESCC cell line) were investigated with Boyden chambers. The results showed that transfection of Stat3 not only promoted invasion of EC-1 cells but also significantly induced MMP2 expression in a dose-dependent manner. In contrast, suppressing expression of endogenous Stat3 mRNA and protein by Stat3 siRNA significantly reduced EC-1 cell invasion and MMP2 expression. A high-affinity Stat3-binding element was localized to the positions of 648-641 bp (TTCTCGAA) in the MMP2 promoter with electrophoretic mobility shift assay. Our results suggest that Stat3, p-Stat3, and MMP2 were overexpressed in ESCC and associated with invasion of ESCC; and Stat3 up-regulated expression of MMP2 in ESCC through directly binding to the MMP2 promoter.

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Section: Discussionmentioning

confidence: 99%

Stat3 promotes invasion of esophageal squamous cell carcinoma through up-regulation of MMP2

Xuan

Lou

et al. 2014

Mol Biol Rep

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“…20 In astrocytic tumours, activated STAT3 appears to be marginally predictive of improved survival. 21 These reports suggest that the prognostic role of STAT3 and activated STAT3 varies in different types of cancer.…”

Section: Stat3 and Cyclin D1 In Astrocytic Tumoursmentioning

confidence: 99%

Increased Signal Transducer and Activator of Transcription 3 (STAT3) and Decreased Cyclin D1 in Recurrent Astrocytic Tumours Compared with Paired Primary Astrocytic Tumours

et al. 2011

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This study compared the levels of signal transducer and activator of transcription 3 (STAT3) and cyclin D1 protein in paired primary and recurrent astrocytic tumours, and analysed their correlation with clinicopathological and treatment factors. A total of 48 samples from 24 patients who had undergone surgical removal of primary and recurrent astrocytic tumours were analysed. Levels of STAT3 and cyclin D1 protein were detected using immunohistochemistry. Increased STAT3 and decreased cyclin D1 levels were observed in recurrent astrocytic tumours compared with their paired primary tumours. There was a significant correlation between higher levels of STAT3 protein and shorter progression-free survival in primary tumours after surgery (r = 0.417), and a significant correlation between decreased cyclin D1 protein levels and radiotherapy in recurrent tumours (r = 0.468). It was concluded that increased STAT3 and decreased cyclin D1 protein levels may contribute to the recurrence of astrocytic tumours. Detection of STAT3 may be useful in predicting progressionfree survival in primary astrocytic tumours after surgery. In addition, radiotherapy may decrease cyclin D1 levels in astrocytic tumours, but the nature of this association requires further investigation.

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“…Signal transducer and activator of transcription (STAT) 3, a member of the STAT protein family, may be activated through phosphorylation by a variety of extracellular growth factors and inflammatory mediators (6). Constitutively activated [phosphorylated (p-)STAT3] was identified in numerous tumor cell lines and a number of human tumors.…”

Section: Introductionmentioning

confidence: 99%

“…Constitutively activated [phosphorylated (p-)STAT3] was identified in numerous tumor cell lines and a number of human tumors. p-STAT3 is significantly associated with tumor invasion and poor prognosis of CRC (6). p-STAT3 exhibits marked expression levels in pancreatic cancer and is associated with tumor staging and metastasis to lymph nodes (6).…”

Section: Introductionmentioning

confidence: 99%

“…p-STAT3 is significantly associated with tumor invasion and poor prognosis of CRC (6). p-STAT3 exhibits marked expression levels in pancreatic cancer and is associated with tumor staging and metastasis to lymph nodes (6). Janus kinase 2 (JAK2) is associated with the embryonic development of normal individuals and is widely expressed in various types of cell, catalyzing the immune responses induced by cytokines (7).…”

Section: Introductionmentioning

confidence: 99%

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Dihydroartemisinin increases apoptosis of colon cancer cells through targeting Janus kinase 2/signal transducer and activator of transcription 3 signaling

et al. 2017

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Abstract. As a derivative of artemisinin, dihydroartemisinin is effective in the treatment of malaria. Dihydroartemisinin has been identified to possess inhibitory effects in numerous types of animal model with tumors, indicating that it has an antineoplastic effect. The aim of the present study was to analyze the potential anticancer effects of dihydroartemisinin, particularly its effect on apoptosis of colon cancer cells. In the present study, it was identified that dihydroartemisinin inhibited cell viability, promoted cell apoptosis, increased B-cell lymphoma-2-associated X-protein expression, increased caspase-3/9 activities, decreased poly(ADP-ribose) polymerase levels, decreased phosphorylation of extracellular-signal-regulated kinase, and increased phosphorylation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase in colon cancer cells. Conversely, the phosphorylation of Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) was suppressed by dihydroartemisinin in colon cancer cells. These results demonstrate that the potential anticancer effects of dihydroartemisinin may increase apoptosis of colon cancer cells through targeting JAK2/STAT3 signaling.

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Prognostic value of phosphorylated STAT3 in advanced rectal cancer: a study from 104 French patients included in the EORTC 22921 trial

Abstract: These results highlight an unexpected role for nuclear p-STAT3 expression in advanced rectal cancers and need further investigation to clarify this finding.

Cited by 28 publications

References 45 publications

Stat3 promotes invasion of esophageal squamous cell carcinoma through up-regulation of MMP2

Stat3 promotes invasion of esophageal squamous cell carcinoma through up-regulation of MMP2

Increased Signal Transducer and Activator of Transcription 3 (STAT3) and Decreased Cyclin D1 in Recurrent Astrocytic Tumours Compared with Paired Primary Astrocytic Tumours

Dihydroartemisinin increases apoptosis of colon cancer cells through targeting Janus kinase 2/signal transducer and activator of transcription 3 signaling

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