IL-32θ inhibits stemness and epithelial-mesenchymal transition of cancer stem cells<i>via</i>the STAT3 pathway in colon cancer

Bak, Yesol; Kwon, Taeho; Bak, In Seon; Jiang, Hong; Yu, Dae‐Yeul; Yoon, Do‐Young

doi:10.18632/oncotarget.7007

Cited by 36 publications

(40 citation statements)

References 36 publications

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“…Colon cancer is among the most common cancers worldwide, and it is the second leading cause of cancer-related deaths. 19 One evidences showed ENO1 expressed aberrantly in multiple tumor types and its expression was associated with disease progression. 11,20,21 However, little is known about the role and mechanism of ENO1 in CRC.…”

Section: Discussionmentioning

confidence: 99%

α‐enolase promotes tumorigenesis and metastasis via regulating AMPK/mTOR pathway in colorectal cancer

Zhan

Zhao

Hua

et al. 2017

Molecular Carcinogenesis

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The α-enolase (ENO1) plays pivotal roles in several types of cancer, but its clinical significance, functional role, and possible mechanism in colorectal cancer (CRC) have remained unclear. Expression level of ENO1 in CRC tissues was examined by qRT-PCR, Western blot, and immunohistochemistry. The effects of ENO1 on cell growth were investigated by MTT, colony formation, flow cytometry assays, and in vivo tumorigenic capacity analysis. The impacts of ENO1 on cell migration and invasion were also explored by scratch-healing, Transwell or Matrigel chamber assays, and in vivo metastatic capacity analysis. Our results showed that the expression level of ENO1 was significantly elevated in CRC tissues. High expression level of ENO1 was associated with disease progression in CRC patients. Overexpression of ENO1 in HCT116 cell line promoted cell proliferation, migration, and invasion in vitro as well as tumorigenesis and metastasis in vivo. In other hand, ablation of ENO1 in HCT116 cells led to totally reverse effects. Mechanistically, we revealed ENO1 could regulate AMPK/mTOR signaling pathway. AMPK pathway activation or mTOR pathway suppression blocked these ENO1 induced alterations. Together, our results demonstrated that ENO1 is a potent promoter of CRC genesis and metastasis at least in part though regulating AMPK/mTOR pathway. These findings also suggested that ENO1 may be a promising therapeutic target in CRC patients.

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Section: Discussionmentioning

confidence: 99%

α‐enolase promotes tumorigenesis and metastasis via regulating AMPK/mTOR pathway in colorectal cancer

Zhan

Zhao

Hua

et al. 2017

Molecular Carcinogenesis

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“…Previously, much research focus has been on trying to understand inflammatory responses within the tumours through tumour interactions with the extracellular matrix, mesenchymal stem cells, immune cells, cancerassociated fibroblasts and tumour-activated macrophages (Criscitiello et al, 2014;Gilkes et al, 2014;Ginestier et al, 2010Ginestier et al, , 2011Li et al, 2012;Lu et al, 2014). A crosstalk between CSCs and their microenvironment via certain cytokines has been demonstrated (Bak et al, 2016;Di Stefano et al, 2010;Sansone et al, 2007;Singh et al, 2013). In 2011, Liu and coworkers reported that BCSCs are regulated by cytokine-related signalling pathways and highlighted the influence IL6 and IL8 production to maintain CSC properties Sansone et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Hypoxia‐induced secretion stimulates breast cancer stem cell regulatory signalling pathways

et al. 2019

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It is well known that tumour cells are dependent on communication with the tumour microenvironment. Previously, it has been shown that hypoxia (HX) induces pronounced, diverse and direct effects on cancer stem cell ( CSC ) qualities in different breast cancer subtypes. Here, we describe the mechanism by which HX‐induced secretion influences the spreading of CSC s. Conditioned media (CM) from estrogen receptor ( ER )‐α‐positive hypoxic breast cancer cell cultures increased the fraction of CSC s compared to normal growth conditions, as determined using sets of CSC assays and model systems. In contrast, media from ER α‐negative hypoxic cell cultures instead decreased this key subpopulation of cancer cells. Further, there was a striking overrepresentation of JAK ‐ STAT ‐associated cytokines in both the ER α‐positive and ER α‐negative linked hypoxic responses as determined by a protein screen of the CM. JAK ‐ STAT inhibitors and knockdown experiments further supported the hypothesis that this pathway is critical for the CSC ‐activating and CSC ‐inactivating effects induced by hypoxic secretion. We also observed that the interleukin‐6‐ JAK 2‐ STAT 3 axis was specifically central for the ER α‐negative hypoxic behaviour. Our results underline the importance of considering breast cancer subtypes in treatments targeting JAK ‐ STAT or HX‐associated processes and indicate that HX is not only a confined tumour biological event, but also influences key tumour properties in widespread normoxic microenvironments.

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“…The driving force of colorectal cancer was recognized as cancer stem cells (CSCs) (O Brien, Pollett, Gallinger, et al, ), which are a small population of cells in solid tumor responsible for the initiation and progression of cancer (Khan et al, ). CSCs were first identified in acute myeloid leukemia and have been found in various types of cancer (Bak, Kwon, Bak, et al, ). Besides, CSCs are considered to be the most crucial factors that contribute to drug resistance, relapse, and metastasis (Visvader & Lindeman, ).…”

Section: Introductionmentioning

confidence: 99%

Phenethyl isothiocyanate inhibits colorectal cancer stem cells by suppressing Wnt/β‐catenin pathway

Chen

Wang

et al. 2018

Phytotherapy Research

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Cancer stem cells (CSCs) are considered to play essential roles in the process of origination, proliferation, migration, and invasion of cancer, and their properties are regulated by Wnt/β-catenin pathway. Phenethyl isothiocyanate (PEITC) is a natural product obtained from cruciferous vegetables with anticancer activities. The present study aimed to investigate the inhibitory effect and the underlying mechanisms of PEITC on colorectal CSCs. In this study, we found that PEITC can significantly reduce the size and number of colorectal cancer cell spheroids in serum-free medium. With increasing PEITC concentrations (10-40 μM), the number of spheroids was reduced to about 10% of the control group, and the percentage of CD133+ cells was decreased by about 3-16 folds. PEITC also decreased the expression of CSC markers. Meanwhile, inhibition of proliferation as well as induction of apoptosis of colorectal CSCs was observed after PEITC treatment. Furthermore, through activating Wnt/β-catenin pathway with LiCl, the inhibitory effects of PEITC on colorectal CSCs were diminished. Our data suggested that PEITC can be an effective inhibitor of colorectal CSCs by targeting Wnt/β-catenin pathway.

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IL-32θ inhibits stemness and epithelial-mesenchymal transition of cancer stem cellsviathe STAT3 pathway in colon cancer

Cited by 36 publications

References 36 publications

α‐enolase promotes tumorigenesis and metastasis via regulating AMPK/mTOR pathway in colorectal cancer

α‐enolase promotes tumorigenesis and metastasis via regulating AMPK/mTOR pathway in colorectal cancer

Hypoxia‐induced secretion stimulates breast cancer stem cell regulatory signalling pathways

Phenethyl isothiocyanate inhibits colorectal cancer stem cells by suppressing Wnt/β‐catenin pathway

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