The effects and mechanisms of blockage of STAT3 signaling pathway on IL-6 inducing EMT in human pancreatic cancer cells in vitro

Huang, Chengdu; Yang, Guangyao; Jiang, Te; Zhu, Gang; Li, H; Qiu, Zhengjun

doi:10.4149/neo_2011_05_396

Cited by 95 publications

(66 citation statements)

References 44 publications

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“…It is reported that both Akt/mTOR and STAT-3 pathways were upstream pathways controlling both EMT and expression of MMP-2 and MMP-9 [15][16][17][18]. Therefore, we wanted to determine whether PI3K/Akt and STAT-3 pathways were activated upon low-concentration capsaicin treatment.…”

Section: Low-concentration Capsaicin Promotes Migration and Invasion mentioning

confidence: 99%

Low-concentration capsaicin promotes colorectal cancer metastasis by triggering ROS production and modulating Akt/mTOR and STAT-3 pathways

Yang

Li²,

Xu³

et al. 2013

neo

103

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Colorectal cancer (CRC), one of the most common human malignancies, is a major public health problem in the developed world. Capsaicin, widely used as a food additive and as an analgesic agent, is a major pungent ingredient of red pepper. Though capsaicin-induced apoptosis was previously reported in cancer cells, relatively little is known about the impact of capsaicin on other aspect of cancer cell behavior. In this study, we demonstrated that treatment with high-concentration of capsaicin (≥ 200 µM for SW480 and CT-26 cell lines; ≥ 25 µM for HCT116 cell line) inhibited CRC cell proliferation in a dose-dependent manner. In spite of no anti-proliferative effect, notably, low-concentration of capsaicin (100 µM for SW480 and CT-26 cell lines; 12.5 µM for HCT116 cell line) enhanced both migratory and invasive capability of these cells, which was validated by both in vitro and in vivo model. Further, we showed that 100 µM capsaicin induced epithelial-to-mesenchymal (EMT), up-regulated expression of MMP-2 and MMP-9, and activated Akt/mTOR and STAT-3 pathways in SW480 cells. Finally, we showed that capsaicin-induced metastasis of CRC cells was mediated by modulating reactive oxygen species (ROS) production. Our findings are considered as a significant step toward a better understanding of capsaicin-associated regulatory network on CRC cells.

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Section: Low-concentration Capsaicin Promotes Migration and Invasion mentioning

confidence: 99%

Low-concentration capsaicin promotes colorectal cancer metastasis by triggering ROS production and modulating Akt/mTOR and STAT-3 pathways

Yang

Li²,

Xu³

et al. 2013

neo

103

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“…However, a significant percentage of gastric cancer patients fail to achieve complete remission, leading to the relapse or poor prognosis [2]. Metastasis has been regarded as an important mechanism underlying tumor relapse after successful surgical resections [3][4][5]. Metastasis is the advanced stage of solid tumor progression and is a multistep process that involves invasion, intravasation, extravasation to distant organs and final growth of the secondary tumor.…”

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confidence: 99%

RKIP inhibits the malignant phenotypes of gastric cancer cells

Zhang

Gu²,

Liu³

et al. 2012

neo

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Raf kinase inhibitor protein (RKIP) is first identified as an interacting partner of Raf-1. RKIP expression is low or absent in several established cell lines derived from metastatic breast cancer, prostate cancer and melanoma cells. However, the functional role of RKIP in gastric cancer remains unclear. In this study, we employed human gastric cancer cell line SGC7901 as a model to reconstitute RKIP expression in gastric cancer cells. The growth curve and soft agar assay showed that RKIP inhibited the growth and clonogenicity of SGC7901 cells. Flow cytometry analysis showed that RKIP inhibited the cell cycle progression and induced the apoptosis of SGC7901 cells. Wound healing and transwell invasion assay showed that RKIP inhibited the migration and invasion of SGC7901 cells. Furthermore, we observed that RKIP inhibited the growth of SMGC7901 cells in xenografts in nude mice. Taken together, our in vitro and in vivo data demonstrate that RKIP modulates the proliferation, apoptosis, migration, invasion and tumorigenicity of SGC7901 cells. These results reveal the tumor suppressor role of RKIP in gastric cancer and suggest that RKIP may be new therapeutic target for gastric cancer. Key words: gastric cancer, RKIP, Raf, tumor suppressor, SGC7901, apoptosisIn the last decade, great progress has been made in the treatment of patients with gastric cancer, one of the most prevalent malignancies in Asia [1]. However, a significant percentage of gastric cancer patients fail to achieve complete remission, leading to the relapse or poor prognosis [2]. Metastasis has been regarded as an important mechanism underlying tumor relapse after successful surgical resections [3][4][5]. Metastasis is the advanced stage of solid tumor progression and is a multistep process that involves invasion, intravasation, extravasation to distant organs and final growth of the secondary tumor. A group of genes, termed metastasis suppressor genes (MSGs), encode for proteins that inhibit various steps of the metastatic cascade [6].Raf kinase inhibitor protein (RKIP) is one of the MSGs that suppress metastasis. RKIP is first identified as an interacting partner of Raf-1 and as a negative regulator of mitogen-activated protein kinase (MAPK) pathway downstream of Raf-1 [7]. RKIP expression is low or absent in several established cell lines derived from metastatic breast cancer, prostate cancer and melanoma cells. Moreover, loss of RKIP has been shown to promote tumor development by conferring radioresistance and chemoresistance [8]. However, the functional role of RKIP in gastric cancer remains unclear.Our preliminary study showed that RKIP expression was low in gastric cancer tissues compared to adjacent normal gastric tissues [9]. Therefore, in this study we used gastric cancer cell line SGC7901 cells as a model to investigate whether and how the loss of RKIP contributes to gastric cancer development. Our results demonstrated that reconstitution of RKIP inhibited the proliferation, clonogenicity, migration and invasion of SGC7901 cells in vitro, ...

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“…The serum levels of IL-6 are usually found to be elevated in NPC patients (46). The role that IL-6 plays in the regulation of the growth and invasion of cancer cells has been well demonstrated in various cancer cells such as human melanoma (194), human ductal breast carcinoma (253), renal cell carcinoma (289), ovarian carcinoma cells (243), human oral squamous carcinoma cells (270), head and neck cancer cells (281), human chondrosarcoma cells (286), and human pancreatic cancer cells (112). Ectopic expression of LMP1 in epithelial cells has been shown to result in increased MMP-9 expression (334).…”

Section: The Molecular Mechanisms Of Ebv Infection and The Effects Onmentioning

confidence: 99%

Potential Therapeutic Molecular Targets for Nasopharyngeal Carcinoma

Chen¹

2012

Carcinogenesis, Diagnosis, and Molecular Targeted Treatment for Nasopharyngeal Carcinoma

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The effects and mechanisms of blockage of STAT3 signaling pathway on IL-6 inducing EMT in human pancreatic cancer cells in vitro

Cited by 95 publications

References 44 publications

Low-concentration capsaicin promotes colorectal cancer metastasis by triggering ROS production and modulating Akt/mTOR and STAT-3 pathways

Low-concentration capsaicin promotes colorectal cancer metastasis by triggering ROS production and modulating Akt/mTOR and STAT-3 pathways

RKIP inhibits the malignant phenotypes of gastric cancer cells

Potential Therapeutic Molecular Targets for Nasopharyngeal Carcinoma

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