Evaluation of potential Stat3-regulated genes in human breast cancer

Hsieh, Fu-Chuan; Cheng, Gong; Lin, Jiayuh

doi:10.1016/j.bbrc.2005.07.075

Cited by 164 publications

(141 citation statements)

References 46 publications

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“…In addition, STAT3 is able to regulate the innate and adaptive immune responses during cancer development (31). Recently, the constitutively activated STAT3 has been reported to induce tumor angiogenesis in various cancers including melanoma, breast cancer, gastric cancer, and hepatocellular carcinoma (3)(4)(5)(6). It is not known if STAT3 signaling contributes to angiogenesis in CRC.…”

Section: Discussionmentioning

confidence: 99%

“…In CRC, studies have shown that some proangiogenic factors, such as VEGFA, MMP2 and FGF2, play important roles in angiogenesis (37)(38)(39). In breast cancer, gastric cancer and hepatocellular carcinoma, STAT3 signaling controls VEGFA expression (4,5,14). In pancreatic cancer, STAT3 signaling regulates the expression of MMP2 (15), and in human melanoma brain metastases, activated Stat3 regulates the expression of FGF2 (3).…”

Section: Discussionmentioning

confidence: 99%

“…Not surprisingly, angiogenesis is a complex multistage process and is regulated by the balance between angiogenic and angiostatic factors (2). Recently, more studies have shown that signaling transduction and activation of transcription 3 (STAT3), a key signaling transduction protein and an oncoprotein, appears to play a central role in modulating angiogenesis in various cancers including melanoma, breast cancer, gastric cancer, and hepatocellular carcinoma (3)(4)(5)(6).…”

mentioning

confidence: 99%

“…In addition to its diverse biological functions involved in cell proliferation, differentiation, apoptosis, inflammation, and oncogenesis, accumulating evidence suggests that STAT3 also plays an important role in angiogenesis in both physiological and pathological situations (7)(8)(9)(10)(11)(12)(13). Several studies have reported that STAT3 directly regulates vascular endothelial growth factor A (VEGFA) expression to induce tumor angiogenesis in breast cancer, gastric cancer and hepatocellular carcinoma (4,5,14). In pancreatic cancer, STAT3-targeting RNA interference (RNAi) inhibits angiogenesis by suppressing the expression of matrix metalloproteinase-2 (MMP2) (15).…”

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confidence: 99%

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Inhibition of STAT3 by RNA interference suppresses angiogenesis in colorectal carcinoma

Qian

Guan

Gao

et al. 2011

Braz J Med Biol Res

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Inhibition of STAT3 by RNA interference suppresses angiogenesis in colorectal carcinoma

Qian

Guan

Gao

et al. 2011

Braz J Med Biol Res

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“…Cell pellets were lysed in RIPA lysis buffer as described previously (Hsieh et al, 2005). Protein concentrations were quantitated using BCA protein assay kit from Pierce, Inc. (Rockford, IL, USA) according to the manufacture's protocol.…”

Section: Western Blotmentioning

confidence: 99%

Stat3 activation in human endometrial and cervical cancers

et al. 2007

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The activation of signal transducer and activator of transcription 3 (Stat3) has been implicated in the oncogenesis of cancer and is regarded as a novel target for cancer therapy. Stat3 is classified as a proto-oncogene, because an activated form of Stat3 can mediate oncogenic transformation in cultured cells and tumour formation in nude mice. The constitutive activation of Stat3 has been frequently detected in various types of human cancers. However, the constitutive activation of Stat3 in endometrial and cervical cancers has not been studied. We examined tyrosine phosphorylation of Stat3 (activated form of Stat3) in multiple endometrial and cervical cancer tissues using tissue microarray slides as well as cancer cell lines to explore the possible activation of Stat3. Our results indicated that elevated phosphorylation of Stat3 was detected in cervical and endometrial cancer cell lines. Our results also showed that elevated levels of phosphorylation of Stat3 protein were detected in the endometrial and cervical cancer specimens. This is the first study to demonstrate that Stat3 is activated in human endometrial and cervical cancer tissues. Immunohistochemical staining showed that activated Stat3 is associated with increased expression of downstream antiapoptotic genes, Bcl-xL, survivin, and Mcl-1 in these tissues. Expression of a dominant-negative Stat3 mutant using adenovirus-mediated gene transfer inhibited cell growth and induced apoptosis in HeLa and SiHa cervical cancer cell lines expressing elevated levels of Stat3 phosphorylation. Further, a JAK/Stat3 small molecular inhibitor, JSI-124, induced apoptosis more selectively in HeLa and SiHa cancer cell lines than Ishikawa cell line without elevated levels of Stat3 phosphorylation. These results indicate that Stat3 is activated in human endometrial and cervical cancers and the inhibition of constitutive Stat3 signaling may be an effective target for cancer intervention in these two cancers.

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RETRACTED: Expression of adrenomedullin in human colorectal tumors and its role in cell growth and invasion in vitro and in xenograft growth in vivo

et al. 2013

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Adrenomedullin (AM) is a multifunctional peptide vasodilator that transduces its effects through calcitonin receptor-like receptor/receptor activity-modifying protein-2 and -3 (CLR/RAMP2 and CLR/RAMP3). In this study, real-time quantitative reverse transcription demonstrated a significant expression of AM mRNA in tumor samples from colorectal cancer (CRC) patients in clinical stage II, III, and IV when compared with normal colorectal tissue. AM, CLR, RAMP2, and RAMP3 proteins were immunohistochemically localized in the carcinomatous epithelial compartment of CRC tissue. Tissue microarray analysis revealed a clear increase of AM, CLR, RAMP2, and RAMP3 staining in lymph node and distant metastasis when compared with primary tumors. The human colon carcinoma cells HT-29 expressed and secreted AM into the culture medium with a significant increase under hypoxia. Treatment of HT-29 cells with synthetic AM stimulated cell proliferation and invasion in vitro. Incubation with anti-AM antibody (αAM), anti-AM receptors antibodies (αAMR), or AM antagonist AM22–52 inhibited significantly basal levels of proliferation of HT-29 cells, suggesting that AM may function as an autocrine growth factor for CRC cells. Treatment with αAM significantly suppressed the growth of HT-29 tumor xenografts in vivo. Histological examination of αAM-treated tumors showed evidence of disruption of tumor vascularity with decreased microvessel density, depletion of endothelial cells and pericytes, and increased tumor cell apoptosis. These findings highlight the potential importance of AM and its receptors in the progression of CRC and support the conclusion that αAM treatment inhibits tumor growth by suppression of angiogenesis and tumor growth, suggesting that AM may be a useful therapeutic target.

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Evaluation of potential Stat3-regulated genes in human breast cancer

Cited by 164 publications

References 46 publications

Inhibition of STAT3 by RNA interference suppresses angiogenesis in colorectal carcinoma

Inhibition of STAT3 by RNA interference suppresses angiogenesis in colorectal carcinoma

Stat3 activation in human endometrial and cervical cancers

RETRACTED: Expression of adrenomedullin in human colorectal tumors and its role in cell growth and invasion in vitro and in xenograft growth in vivo

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