Stromal COX-2 signaling are correlated with colorectal cancer: A review

Su, Chen‐Wei; Zhang, Yuan; Zhu, Yingting

doi:10.1016/j.critrevonc.2016.08.010

Cited by 31 publications

(28 citation statements)

References 60 publications

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“…Cyclooxygenase‐2 in tumor‐associated macrophages (TAMs) promotes breast cancer metastasis through the induction of MMP9 and the promotion of EMT in tumor cells 43 . In addition, cancer‐associated fibroblasts (CAFs) are major sources of COX‐2/PGE 2 in the tumor microenvironment 44 . These results suggest that the regulation of EMT by PGE 2 produced from TAMs, CAFs, or tumors, could further promote tumor metastasis.…”

Section: Discussionmentioning

confidence: 99%

Epidermal growth factor‐induced COX‐2 regulates metastasis of head and neck squamous cell carcinoma through upregulation of angiopoietin‐like 4

et al. 2020

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Epidermal growth factor receptor (EGFR) expression and activation are the major causes of metastasis in cancers such as head and neck squamous cell carcinoma (HNSCC). However, the reciprocal effect of EGF‐induced COX‐2 and angiopoietin‐like 4 (ANGPTL4) on HNSCC metastasis remains unclear. In this study, we revealed that the expression of ANGPTL4 is essential for COX‐2‐derived prostaglandin E2 (PGE2)‐induced tumor cell metastasis. We showed that EGF‐induced ANGPTL4 expression was dramatically inhibited with the depletion and inactivation of COX‐2 by knockdown of COX‐2 and celecoxib treatment, respectively. Prostaglandin E2 induced ANGPTL4 expression in a time‐ and dose‐dependent manners in various HNSCC cell lines through the ERK pathway. In addition, the depletion of ANGPTL4 and MMP1 significantly impeded the PGE2‐induced transendothelial invasion ability of HNSCC cells and the binding of tumor cells to endothelial cells. The induction of molecules involved in the regulation of epithelial‐mesenchymal transition was also dependent on ANGPTL4 expression in PGE2‐treated cells. The depletion of ANGPTL4 further blocked PGE2‐primed tumor cell metastatic seeding of lungs. These results indicate that the EGF‐activated PGE2/ANGPTL4 axis enhanced HNSCC metastasis. The concurrent expression of COX‐2 and ANGPTL4 in HNSCC tumor specimens provides insight into potential therapeutic targets for the treatment of EGFR‐associated HNSCC metastasis.

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Section: Discussionmentioning

confidence: 99%

Epidermal growth factor‐induced COX‐2 regulates metastasis of head and neck squamous cell carcinoma through upregulation of angiopoietin‐like 4

et al. 2020

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“…In this regard, the transcriptional modulator CCAAT/enhancer binding protein‐β (C/EBP‐β) takes part in the effector pathways of metabolic reprogramming that promotes the loss of E‐cadherin during EMT . The overexpression of C/EBP‐β controls the cycle of tumor progression, as reported in gastric adenocarcinoma AGS cells, where C/EBP‐β activated NF‐κB and further positively regulated the proinflammatory COX‐2, an upregulated enzyme in gastric cancer and CRC . Interestingly, in gastric carcinogenesis the initiation of melatonin treatment markedly inhibited the C/EBP‐β/NF‐κB cascade, reducing the binding affinity of C/EBP‐β and NF‐κB to the promoter of COX‐2 gene, thus leading to the reduction of constitutive expression of proangiogenic and tumorigenic chemokines that facilitate tumor growth, peritoneal dissemination, and implantation of distant metastases .…”

Section: Multimodal Approach Using Melatonin Against Progression and mentioning

confidence: 99%

“…Since the aforementioned epidemiological, observational, and experimental studies, the intricate molecular relationship between inflammation, CRC, and melatonin begins to become apparent. The inducible isoform of cyclooxigenase‐2 (COX‐2) is a rate‐limiting enzyme for prostaglandin production, induced by several proinflammatory cytokines, growth factors, and tumor promoters, and which is involved, just like multifunctional prostaglandins, in inflammation and colorectal carcinogenesis . Furthermore, the role of COX‐2 in colorectal carcinogenesis is associated with the activation of inducible nitric oxide synthase (iNOS) .…”

Section: Multimodal Approach Using Melatonin Against Progression and mentioning

confidence: 99%

“…The inducible isoform of cyclooxigenase-2 (COX-2) is a rate-limiting enzyme for prostaglandin production, induced by several proinflammatory cytokines, growth factors, and tumor promoters, and which is involved, just like multifunctional prostaglandins, in inflammation and colorectal carcinogenesis. 131 Furthermore, the role of COX-2 in colorectal carcinogenesis is associated with the activation of inducible nitric oxide synthase (iNOS). 132 Consequently, the design of or identification of new specific COX-2 and iNOS inhibitors could be a valuable strategy for the treatment of inflammation and the associated CRC.…”

Section: How Melatonin Brakes the Alliance Between Intestinal Inflamentioning

confidence: 99%

“…230 The overexpression of C/EBP-β controls the cycle of tumor progression, as reported in gastric adenocarcinoma AGS cells, where C/EBP-β activated NF-κB and further positively regulated the proinflammatory COX-2, 183,231 an upregulated enzyme in gastric cancer 232 and CRC. 131,233 Interestingly, in gastric carcinogenesis the initiation of melatonin treatment markedly inhibited the C/EBP-β/NF-κB cascade, reducing the binding affinity of C/EBP-β and NF-κB to the promoter of GIL-MARTÍN ET AL.…”

Section: The Influence Of Melatonin On the Molecular Mechanisms Of mentioning

confidence: 99%

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The emergence of melatonin in oncology: Focus on colorectal cancer

Gil‐Martín

Egea

Reíter

et al. 2019

Medicinal Research Reviews

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Within the last few decades, melatonin has increasingly emerged in clinical oncology as a naturally occurring bioactive molecule with substantial anticancer properties and a pharmacological profile optimal for joining the currently available pharmacopeia. In addition, extensive experimental data shows that this chronobiotic agent exerts oncostatic effects throughout all stages of tumor growth, from initial cell transformation to mitigation of malignant progression and metastasis; additionally, melatonin alleviates the side effects and improves the welfare of radio/chemotherapy‐treated patients. Thus, the support of clinicians and oncologists for the use of melatonin in both the treatment and proactive prevention of cancer is gaining strength. Because of its epidemiological importance and symptomatic debut in advanced stages of difficult clinical management, colorectal cancer (CRC) is a preferential target for testing new therapies. In this regard, the development of effective forms of clinical intervention for the improvement of CRC outcome, specifically metastatic CRC, is urgent. At the same time, the need to reduce the costs of conventional anti‐CRC therapy results is also imperative. In light of this status quo, the therapeutic potential of melatonin, and the direct and indirect critical processes of CRC malignancy it modulates, have aroused much interest. To illuminate the imminent future on CRC research, we focused our attention on the molecular mechanisms underlying the multiple oncostatic actions displayed by melatonin in the onset and evolution of CRC and summarized epidemiological evidence, as well as in vitro, in vivo and clinical findings that support the broadly protective potential demonstrated by melatonin.

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MiR‐216a‐3p inhibits colorectal cancer cell proliferation through direct targeting COX‐2 and ALOX5

Wang¹,

Li²,

Zhang³

et al. 2017

J of Cellular Biochemistry

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Colorectal Cancer (CRC) is a most common digestive system malignant tumor. Despite recent advance in CRC treatment, searching for efficient biomarker and individual treatment therapy remains an urgent need. Cyclooxygenase-2 (COX-2) plays a critical role in the development and progression of CRC. In addition, shunting of arachidonic acid metabolism to the 5-lipoxygenase (ALOX5, 5-LO) pathway has also been reported to be implicated in the CRC pathogenesis. Cancer cell viability is promoted by ALOX5 through several mechanisms that are similar to those of COX-2. In recent years, it has been widely recognized that through inhibition of target genes, miRNAs can exert both oncogenic and tumor suppressive functions, depending on circumstances. In the present study, we screened for candidate microRNAs (miRNAs) which were predicted to regulate COX-2 and ALOX5 by online tools. Among the candidate miRNAs, miR-216a-3p expression was down-regulated in CRC tissues and cell lines; a higher miR-216a-3p expression was correlated with longer overall survival in patients with CRC. Moreover, ectopic miR-216a-3p expression significantly suppressed CRC cell proliferation. Using luciferase reporter gene, real-time PCR, and western blot assays, we confirmed the miR-216a-3p regulation of COX-2 and ALOX5 through direct targeting; further verified that miR-216a-3p could inhibit COX-2 and ALOX5 expression in CRC cells, thus to affect CRC cell proliferation. Taken together, miR-216a-3p presents a novel target of CRC treatment; rescuing miR-216a-3p expression in CRC might be a promising strategy for CRC treatment.

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Stromal COX-2 signaling are correlated with colorectal cancer: A review

Cited by 31 publications

References 60 publications

Epidermal growth factor‐induced COX‐2 regulates metastasis of head and neck squamous cell carcinoma through upregulation of angiopoietin‐like 4

Epidermal growth factor‐induced COX‐2 regulates metastasis of head and neck squamous cell carcinoma through upregulation of angiopoietin‐like 4

The emergence of melatonin in oncology: Focus on colorectal cancer

MiR‐216a‐3p inhibits colorectal cancer cell proliferation through direct targeting COX‐2 and ALOX5

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