Cell–cell contacts induce STAT3 activity in colon carcinoma cells through an autocrine stimulation loop

Tsareva, Svetlana A.; Wagner, Stefan; Müller, Annekatrin; Corvinus, Florian; Friedrich, Karlheinz

doi:10.1007/s00432-010-0943-3

Cited by 4 publications

(3 citation statements)

References 21 publications

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“…[1][2][3] In in vitro studies, the autocrine cytokines or chemokines from tumor cells in the conditioned medium (CM) showed profound effects on progression of tumor cells. 4,5 Glioma is the most common form of primary malignant brain cancers and tumor cell invasiveness is a critical challenge in the management of glioma. The invasive biological feature of glioma cells has a complex mechanism and involves several well orchestrated signaling pathways stimulated by both autocrine and paracrine factors that act on various cell surface-bound receptors including G-protein coupled receptor (GPCR).…”

Section: Introductionmentioning

confidence: 99%

Autocrine IL-8 promotes F-actin polymerization and mediate mesenchymal transition via ELMO1-NF-κB-Snail signaling in glioma

Zhang

Shi

et al. 2015

Cancer Biology & Therapy

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Section: Introductionmentioning

confidence: 99%

Autocrine IL-8 promotes F-actin polymerization and mediate mesenchymal transition via ELMO1-NF-κB-Snail signaling in glioma

Zhang

Shi

et al. 2015

Cancer Biology & Therapy

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“…STAT3 regulates the transcription of MMP-1, which has been reported in colon cancer. STAT3 may directly act on MMP-1 or indirectly facilitate MMP-1 expression via activator protein (AP)-1 (a transcription factor) (11,25).…”

Section: Discussionmentioning

confidence: 99%

Expression of STAT3, MMP-1 and TIMP-1 in gastric cancer and correlation with pathological features

Cai

Wang

et al. 2012

Mol Med Report

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Abstract. The aim of this study was to investigate the mRNA and protein expression of STAT3, MMP-1 and TIMP-1 in gastric cancer (GC), and to explore the correlations between these proteins and the biological behaviors of GC. Reverse transcription-polymerase chain reaction was employed to detect the mRNA expression of STAT3, MMP-1 and TIMP-1 in GC tissues (n=30), adjacent normal tissues (n=30) and superficial gastritis (SG) tissues (n=30). Immunohistochemistry was performed using the SP method to measure the protein expression of STAT3 (unphosphorylated), MMP-1 and TIMP-1. The correlation between the pathological features of GC and STAT3, MMP-1 as well as TIMP-1, were evaluated. The mRNA expression of STAT3 in GC tissues (0.821±0.128) was significantly higher compared to that in adjacent normal tissues (0.355±0.100) and SG tissues (0.398±0.096) (P<0.05). The mRNA expression of MMP-1 in GC tissues (0.749±0.133) was significantly increased compared to adjacent normal tissues (0.335±0.106) and SG tissues (0.345±0.063) (P<0.05). The mRNA expression of TIMP-1 in GC tissues (0.386±0.125) was comparable to that in adjacent normal tissues (0.343±0.078) and SG tissues (0.345±0.061), but the mRNA expression of TIMP-1 in GC tissues was significantly correlated with the differentiation of GC cells and lymph node metastasis. STAT3, MMP-1 and TIMP-1 were significantly associated with the differentiation of GC cells and lymph node metastasis, but not related to age, gender and tumor size. The positive rate of unphosphorylated STAT3 expression was dramatically higher in GC tissues (86.7%) compared to that in adjacent normal tissues (16.7%) and SG tissues (10.0%) (P<0.05). The positive rate of MMP-1 protein expression in GC tissues (63.3%) was significantly higher compared to that in adjacent normal tissues (13.3%) and SG tissues (16.7%) (P<0.05). However, no significant difference was observed in the TIMP-1-positive rate among the three groups (23.3, 16.7 and 10.0%, respectively; P>0.05). STAT3 and MMP-1 may be involved in the development and metastasis of GC, and treatment targeting TIMP-1 may be a promising strategy.

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“…The phosphorylated tyrosine binds reversibly to the SH2 region of another STAT3 monomer to form the STAT3 homodimer, which can translocate to the nucleus, where it functions as a transcription factor and promotes gene transcription, regulates tumor cell cycle progression and inhibits apoptosis. 12,13 In addition, 5-FU resistance was shown to be reduced by inhibiting the JAK2/STAT3 pathway. 14 There is no such report on the interaction between CPT and JAK2/STAT3 in GC, despite an increasing number of reports implicating JAK2/STAT3 and CPT in GC proliferation.…”

Section: Introductionmentioning

confidence: 99%

Cryptotanshinone From Salvia miltiorrhiza Inhibits the Growth of Tumors and Enhances the Efficacy of Chemotherapy in a Gastric Cancer Mouse Model

Cao

Liu

et al. 2022

Natural Product Communications

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Cryptotanshinone is a quinone diterpene extracted from the traditional Chinese medicine Salvia miltiorrhiza root that shows obvious anticancer activity. The aim of this study was to investigate the mechanism of action of cryptotanshinone as an antigastric cancer agent, as well as a chemotherapy potentiator. A gastric cancer model was established by tumor transplantation, and mice were treated with either 5-fluorouracil or cryptotanshinone, or both drugs. The tumor mass was recorded, and the tumor suppression rate was calculated. Pathological changes were observed by hematoxylin and eosin staining, gene transcription was detected by quantitative polymerase chain reaction, and protein expression by Western blotting. The results showed that cryptotanshinone could reduce the tumor mass, increase the tumor suppression rate, and enhance the chemotherapeutic effect of 5-fluorouracil by a mechanism related to inhibition of the Janus kinase 2/signal transducer and activator of transcription 3 signaling pathway.

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Cell–cell contacts induce STAT3 activity in colon carcinoma cells through an autocrine stimulation loop

Abstract: Changing cultivation conditions of the CRC cell line HT-29 toward detachment and aggregation, thus toward the situation in tumors, induces STAT3 activity and evokes an autocrine STAT3 activation loop.

Cited by 4 publications

References 21 publications

Autocrine IL-8 promotes F-actin polymerization and mediate mesenchymal transition via ELMO1-NF-κB-Snail signaling in glioma

Autocrine IL-8 promotes F-actin polymerization and mediate mesenchymal transition via ELMO1-NF-κB-Snail signaling in glioma

Expression of STAT3, MMP-1 and TIMP-1 in gastric cancer and correlation with pathological features

Cryptotanshinone From Salvia miltiorrhiza Inhibits the Growth of Tumors and Enhances the Efficacy of Chemotherapy in a Gastric Cancer Mouse Model

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