ESM-1 regulates cell growth and metastatic process through activation of NF-κB in colorectal cancer

Kang, Yun Hee; Ji, Na; Han, Seung Ro; Lee, Chung Il; Kim, Jae Wha; Yeom, Young Il; Kim, Young Ho; Chun, Ho Kyung; Kim, Jong Wan; Chung, Jin Woong; Ahn, Dong Kuk; Lee, Hee Gu; Song, Eun Young

doi:10.1016/j.cellsig.2012.06.004

Cited by 74 publications

(86 citation statements)

References 31 publications

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“…By contrast, phosphorylated ERK1, GSK α/β and p38α expression levels were decreased and phospho-p38δ, -RSK1, -Akt1, -pan-Akt and -HSP27 were not detected in ESM-1 knockdown cells (25). In colorectal cancer, the interactions of endocan, NF-κB activation and NF-κB promoter are involved in cell survival, cell cycle progression, migration, invasion and tumor invasion epithelial-mesenchymal transition (EMT) (25). Akt-dependent NF-κB is suppressed in ESM-1 siRNA-expressing COLO205 cells, indicating that ESM-1 increased the COLO205 cell survival rate via the Akt-dependent NF-κB/IκB pathway (25).…”

Section: Endocan As a New Marker Of Cancer And Target For Cancer Therapymentioning

confidence: 82%

“…The c-Jun N-terminal kinase, ERK and p38 pathways are not directly associated with the suppression of survival in ESM-1 siRNA-expressing COLO205 cells, indicating that ESM-1 may affect COLO205 cell survival via the Akt-dependent NF-κB/IκB pathway, rather than other survival-related pathways (25). ESM-1 gene silencing regulates cell cycle arrest by phosphatase and tensin homolog (PTEN) induction, and PTEN-induced growth suppression in COLO205 cells (25). Endocan is known to influence cell invasion (25), and ESM-1 siRNA-expressing cells had a cell invasion rate of 1.35-fold less than those expressing control siRNA.…”

Section: Endocan As a New Marker Of Cancer And Target For Cancer Therapymentioning

confidence: 94%

“…Akt-dependent NF-κB is suppressed in ESM-1 siRNA-expressing COLO205 cells, indicating that ESM-1 increased the COLO205 cell survival rate via the Akt-dependent NF-κB/IκB pathway (25). The c-Jun N-terminal kinase, ERK and p38 pathways are not directly associated with the suppression of survival in ESM-1 siRNA-expressing COLO205 cells, indicating that ESM-1 may affect COLO205 cell survival via the Akt-dependent NF-κB/IκB pathway, rather than other survival-related pathways (25). ESM-1 gene silencing regulates cell cycle arrest by phosphatase and tensin homolog (PTEN) induction, and PTEN-induced growth suppression in COLO205 cells (25).…”

Section: Endocan As a New Marker Of Cancer And Target For Cancer Therapymentioning

confidence: 96%

“…Phosphorylated extracellular signal-regulated kinase 1 (ERK1), glycogen synthase kinase (GSK) α/β, p38 α/δ, ribosomal S6 kinase 1 (RSK1), Akt1, pan-Akt and heat-shock protein 27 (HSP27) were highly expressed in cells transfected with the control siRNA. By contrast, phosphorylated ERK1, GSK α/β and p38α expression levels were decreased and phospho-p38δ, -RSK1, -Akt1, -pan-Akt and -HSP27 were not detected in ESM-1 knockdown cells (25). In colorectal cancer, the interactions of endocan, NF-κB activation and NF-κB promoter are involved in cell survival, cell cycle progression, migration, invasion and tumor invasion epithelial-mesenchymal transition (EMT) (25).…”

Section: Endocan As a New Marker Of Cancer And Target For Cancer Therapymentioning

confidence: 99%

“…In colorectal cancer, the interactions of endocan, NF-κB activation and NF-κB promoter are involved in cell survival, cell cycle progression, migration, invasion and tumor invasion epithelial-mesenchymal transition (EMT) (25). Akt-dependent NF-κB is suppressed in ESM-1 siRNA-expressing COLO205 cells, indicating that ESM-1 increased the COLO205 cell survival rate via the Akt-dependent NF-κB/IκB pathway (25). The c-Jun N-terminal kinase, ERK and p38 pathways are not directly associated with the suppression of survival in ESM-1 siRNA-expressing COLO205 cells, indicating that ESM-1 may affect COLO205 cell survival via the Akt-dependent NF-κB/IκB pathway, rather than other survival-related pathways (25).…”

Section: Endocan As a New Marker Of Cancer And Target For Cancer Therapymentioning

confidence: 99%

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Endocan: A new marker for cancer and a target for cancer therapy

Yang

et al. 2015

Biomedical Reports

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Abstract. Endocan, previously known as endothelial cell-specific molecule-1 (ESM-1), was cloned from the human umbilical vein endothelial cell cDNA library. Endocan is a novel ESM, and a 50 kDa soluble proteoglycan. Endocan is secreted into the blood as the soluble proteoglycan, which is the form in the presence of chondroitin sulfate. In normal tissues, chondroitin sulfate/dermatan sulfate proteoglycan is expressed by endothelial cells (such as lung and kidney) and is overexpressed in several carcinoma endothelial cells. There are studies that identified high endocan expression in lung cancer, uterine cancer, kidney cancer, liver cancer, brain glioblastoma, breast cancer and other tumors. Tumor prognosis, metastasis and angiogenesis were shown to be associated with endocan expression. The majority of investigators believe that endocan regulates the tumor by tumor-associated inflammation, angiogenesis, lymphangiogenesis, the tumor cells themselves and other aspects. Endocan may be a new target for cancer therapy.

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Section: Endocan As a New Marker Of Cancer And Target For Cancer Therapymentioning

confidence: 82%

Section: Endocan As a New Marker Of Cancer And Target For Cancer Therapymentioning

confidence: 94%

Section: Endocan As a New Marker Of Cancer And Target For Cancer Therapymentioning

confidence: 96%

Section: Endocan As a New Marker Of Cancer And Target For Cancer Therapymentioning

confidence: 99%

Section: Endocan As a New Marker Of Cancer And Target For Cancer Therapymentioning

confidence: 99%

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Endocan: A new marker for cancer and a target for cancer therapy

Yang

et al. 2015

Biomedical Reports

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The Role of Phenethyl Isothiocyanate on Bladder Cancer ADM Resistance Reversal and Its Molecular Mechanism

Tang

Lin

2013

The Anatomical Record

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Adramycin (ADM) resistance is an essential aspect of bladder cancer treatment failure and phenethyl isothiocyanate (PEITC) has been found to exhibit antitumor properties; however, the effect and potential mechanism of PEITC on bladder cancer ADM resistance reversal is not fully clear. The aim of this study was to explore the role of PEITC in bladder cancer cells ADM resistance reversal and the underlying molecular mechanisms. In this report, we identified the role of PEITC on ADM resistance reversal of human bladder carcinoma T24/ADM cells, including an increased drug sensitivity to ADM, cell apoptosis rates, intracellular accumulation of , an increased expression of DNA topoisomerase II (Topo-II), and a decreased expression of multidrug resistance gene (MDR1), multidrug resistance-associated protein (MRP1), bcl-2 and glutathione s transferase p (GST-p).We also found that there was a decreased expression of NF-jB, Survivin, Twist, and p-Akt, and an increased expression of PTEN and p-JNK after PEITC treatment for T24/ ADM cells. The results indicated that PEITC might be used as a potential therapeutic strategy to ADM resistance through blocking Akt and activating MAPK pathway in human bladder carcinoma. Anat Rec, 296:899-906, 2013. V C 2013 Wiley Periodicals, Inc. Key words: adramycin; bladder cancer; drug resistanceBladder cancer is one of the most common malignant tumors which are threatening human's life and health seriously (Oosterlinck and Decaestecker, 2012). Surgery assisted by chemotherapy has become the main therapeutic schemes for bladder cancer. Reasonable chemotherapy could use the anti-cancer drugs cytotoxicity to the maximum, but bladder cancer was palindromic in the biological characteristics, and its relapse rate has been high. One of the reasons was the generation of anti-cancer drug resistance. Therefore, the resistance of anti-cancer drug has become a major obstacle in the chemotherapy of bladder cancer, and it must clarify the drug resistance mechanisms to eliminate the anti-cancer drug resistance of tumor cells. Like most malignant bladder cancer, it showed multidrug resistance (Multidrug Resistance, MDR) in anticancer drug resistance. Resistance mechanisms of tumor cells was quite complex, and summarized the followings: (1) drug transporting or uptaking barriers; (2) drug activation barriers; (3) target enzyme changes in the quantity and quality; (4) metabolic pathways increased; (5) decomposing enzyme increased; (6) repair mechanisms increased; (7) the cell membrane glycoprotein specific in excluding drugs increased; (8) DNA chains cross-linked reduced; (9) hormone receptor reduction or loss of function, and so on (Kunze et al., 2012).The generation of multidrug resistance in tumor cells has become a major cause of failure in tumor

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Tumor DNA‐methylome derived epigenetic fingerprint identifies HPV‐negative head and neck patients at risk for locoregional recurrence after postoperative radiochemotherapy

Tawk

Wirkner

Schwager

et al. 2021

Intl Journal of Cancer

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Biomarkers with relevance for loco-regional therapy are needed in human papillomavirus negative aka HPV(À) head and neck squamous cell carcinoma (HNSCC). Based on the premise that DNA methylation pattern is highly conserved, we sought to develop a reliable and robust methylome-based classifier identifying HPV(À) HNSCC patients at risk for loco-regional recurrence (LR) and all-event progression after postoperative radiochemotherapy (PORT-C). The training cohort consisted of HPV-DNA negative HNSCC patients (n = 128) homogeneously treated with PORT-C in frame of the German Cancer Consortium-Radiation Oncology Group (DKTK-ROG) multicenter biomarker trial. DNA Methylation analysis was performed using Illumina 450 K and 850 K-EPIC microarray technology. The performance of the classifier was integrated with a series of biomarkers studied in the training set namely hypoxia-, 5-microRNA (5-miR), stem-cell gene-expression signatures and immunohistochemistry (IHC)-based immunological characterization of tumors (CD3/CD8/PD-L1/PD1). Validation occurred in an independent cohort of HPV(À) HNSCC patients, pooled from two German centers (n = 125). We identified a 38-methylation probe-based HPV(À)

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ESM-1 regulates cell growth and metastatic process through activation of NF-κB in colorectal cancer

Cited by 74 publications

References 31 publications

Endocan: A new marker for cancer and a target for cancer therapy

Endocan: A new marker for cancer and a target for cancer therapy

The Role of Phenethyl Isothiocyanate on Bladder Cancer ADM Resistance Reversal and Its Molecular Mechanism

Tumor DNA‐methylome derived epigenetic fingerprint identifies HPV‐negative head and neck patients at risk for locoregional recurrence after postoperative radiochemotherapy

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