Celecoxib as an adjuvant to chemotherapy for patients with metastatic colorectal cancer

Mostafa, Tarek; El-Din, Mohamed A. Alm; Rashdan, Amira R.

doi:10.15537/smj.2022.43.1.20210574

Cited by 10 publications

(8 citation statements)

References 30 publications

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“…VEGFA is an important molecule of VEGF protein family, which could activate downstream signaling pathways by interacting with VEGF Receptor 2 (VEGFR-2), leading to normal angiogenesis or abnormal lesions [18,19] . VEGF could induce ERK molecule and further activate the endothelial cells after primary cerebral hypoxia and glucose deprivation, resulting in cell damage [20] .…”

Section: Resultsmentioning

confidence: 99%

Peiyuan-Huayu Formula Suppresses Proliferation Migration and Angiogenesis of Human Microvascular Endothelial Cells-1 Through Activating MEK/ERK Signaling Pathway

Fan¹,

Liang²,

Zhao³

et al. 2022

IJPS

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Chronic subdural hematoma is identified as an intracranial hemorrhagic disorder of human. Presently, neither surgical nor symptomatic treatment of Western medicine has achieved good curative effects. This study aimed to clarify efficacy of Peiyuan-Huayu formula on neovascularization and explore associated mechanisms. Rats were intragastricly administrated with Peiyuan-Huayu formula and drug containing serum was harvested. Cell counting kit 8 assay was used to determine proliferation of human microvascular endothelial-1 cells. Human microvascular endothelial-1 cells were divided into negative group, blank-serum group and drug-serum group. In vitro scratch healing assay was employed to evaluate migration distance of human microvascular endothelial cells-1. Tube-like structures formation based on human microvascular endothelial-1 cells was conducted using tube formation assay on matrigel. Expression of vascular endothelial growth factor A, mitogen-activated protein kinase kinase, phosphorylation of mitogen-activated protein kinase kinase and phosphorylation of extracellular signal-regulated kinase was determined with western blotting. The 15 % drug-serum is optimal concentration for inhibiting human microvascular endothelial cells-1 proliferation. Peiyuan-Huayu formula drug-serum remarkably inhibited migration of human microvascular endothelial cells compared to Blank-serum group (p<0.05). Peiyuan-Huayu formula drug-serum obviously suppressed angiogenesis compared to blank-serum group (p<0.05). Peiyuan-Huayu formula drug-serum down-regulated vascular endothelial growth factor A expression, activated phosphorylation of mitogenactivated protein kinase kinase and induced phosphorylation of extracellular signal-regulated kinase 1/2 in human microvascular endothelial-1 cells. In conclusion, Peiyuan-Huayu formula inhibited proliferation, migration and angiogenesis of human microvascular endothelial-1 cells. Effects of Peiyuan-Huayu formula were mediated by reducing expression of mitogen-activated protein kinase kinase 1/2, phosphorylation of mitogen-activated protein kinase kinase 1/2, phosphorylation of extracellular signal-regulated kinase 1/2 and vascular endothelial growth factor molecule.

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Section: Resultsmentioning

confidence: 99%

Peiyuan-Huayu Formula Suppresses Proliferation Migration and Angiogenesis of Human Microvascular Endothelial Cells-1 Through Activating MEK/ERK Signaling Pathway

Fan¹,

Liang²,

Zhao³

et al. 2022

IJPS

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“…[ 186 ] Clinically, due in part to toxicity concerns (GI and cardiac), COX-2 inhibitors have not been aggressively studied for chemoprevention and cancer therapy [ 187 ]. Recently an adjuvant trial of celecoxib for patients with metastatic CRC was reported [ 188 ]. In this small randomized study, 54 patients with metastatic CRC were randomized into 2 groups: a control group that received 6 cycles of the FOLFIRI regimen as compared to a FOLFIRI and celecoxib group (receiving 6 cycles of FOLFIRI plus 200 mg twice daily of celecoxib over 3 months).…”

Section: Attenuation Of Mdsc Functionmentioning

confidence: 99%

Role of myeloid-derived suppressor cells in tumor recurrence

Cole

Al-Kadhimi

Talmadge

2023

Cancer Metastasis Rev

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The establishment of primary tumor cells in distant organs, termed metastasis, is the principal cause of cancer mortality and is a crucial therapeutic target in oncology. Thus, it is critical to establish a better understanding of metastatic progression for the future development of improved therapeutic approaches. Indeed, such development requires insight into the timing of tumor cell dissemination and seeding of distant organs resulting in occult lesions. Following dissemination of tumor cells from the primary tumor, they can reside in niches in distant organs for years or decades, following which they can emerge as an overt metastasis. This timeline of metastatic dormancy is regulated by interactions between the tumor, its microenvironment, angiogenesis, and tumor antigen-specific T-cell responses. An improved understanding of the mechanisms and interactions responsible for immune evasion and tumor cell release from dormancy would help identify and aid in the development of novel targeted therapeutics. One such mediator of dormancy is myeloid derived suppressor cells (MDSC), whose number in the peripheral blood (PB) or infiltrating tumors has been associated with cancer stage, grade, patient survival, and metastasis in a broad range of tumor pathologies. Thus, extensive studies have revealed a role for MDSCs in tumor escape from adoptive and innate immune responses, facilitating tumor progression and metastasis; however, few studies have considered their role in dormancy. We have posited that MDSCs may regulate disseminated tumor cells resulting in resurgence of senescent tumor cells. In this review, we discuss clinical studies that address mechanisms of tumor recurrence including from dormancy, the role of MDSCs in their escape from dormancy during recurrence, the development of occult metastases, and the potential for MDSC inhibition as an approach to prolong the survival of patients with advanced malignancies. We stress that assessing the impact of therapies on MDSCs versus other cellular targets is challenging within the multimodality interventions required clinically.

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“…Fibroblasts make up the majority of mesenchymal cells, and fibroblasts from non-neoplastic colorectal tissue are an important source of COX-2 expression, which is well-established as a crucial process in the development of CRC [8]. Aspirin and other NSAIDs have been investigated in numerous recent trials for chemoprevention of CRC [15][16][17][18][19][20][21][22][23][24]. It is possible that COX-1 activity in activated platelets serves as a signal to induce COX-2 expression by blocking the release of paracrine lipid and protein mediators that induce COX-2 expression.…”

Section: Cox-2 Enzyme In Colorectal Carcinogenesismentioning

confidence: 99%

“…This finding suggests that celecoxib may have anti-angiogenic properties. The ability of celecoxib to inhibit the COX-2 enzyme with subsequent decreased PGE2, which plays a crucial role in the generation of VEGF, may be the cause of the suppression of angiogenesis translated by decreased VEGF levels by the concurrent use of celecoxib with FOLFIRI [ 23 ]. When compared to sporadic forms, COX inhibition has shown statistically significant results in lowering the risk of familial CRC [ 4 ].…”

Section: Reviewmentioning

confidence: 99%

“…COX-2 inhibitors have been shown to have chemopreventive properties in both preclinical and clinical studies [15][16][17][18]. Consequently, studies have been conducted to evaluate how specific COX-2 inhibitors, such as celecoxib and rofecoxib, affect the growth of adenomas and assist in disease management [19][20][21][22][23][24]. Elevated prostaglandin levels, particularly prostaglandin E2 (PGE2), are commonly observed in individuals with cancer.…”

Section: Introductionmentioning

confidence: 99%

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Protective Effects of Long-Term Usage of Cyclo-Oxygenase-2 Inhibitors on Colorectal Cancer in Genetically Predisposed Individuals and Their Overall Effect on Prognosis: A Systematic Review

Narayana,

Mushtaq,

Shaman Ameen

et al. 2023

Cureus

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Colorectal cancer (CRC) is a major global health concern, accounting for significant cancer-related morbidity and mortality worldwide. Despite advancements in early detection and treatment modalities, the prevention of CRC remains a critical goal. Cyclo-oxygenase-2 (COX-2) is an inducible enzyme involved in the production of pro-inflammatory prostaglandins, which play a crucial role in various cellular processes, including inflammation, cell proliferation, apoptosis, and angiogenesis. Elevated COX-2 expression has been consistently observed in colorectal tumors, indicating their role in the pathogenesis of cancer. COX-2 inhibitors, such as celecoxib and rofecoxib, have been studied as potentially effective treatment modalities due to their ability to decrease prostaglandin levels, which are generally higher in cancer patients. Aberrant prostaglandin production is linked to the adenoma-carcinoma sequence, during which adenomas turn dysplastic and accumulate enough damage to become malignant. COX-2 inhibitors have also been shown to modulate various signaling pathways involved in CRC development, such as wingless-related integration site/β-catenin (Wnt/β-catenin), mitogen-activated protein kinase (MAPK), and phosphoinositide-3-kinaseprotein kinase B/Akt (PI3K/Akt) pathways. This systematic review aimed to evaluate the protective effects of long-term usage of COX-2 inhibitors on CRC in genetically predisposed individuals and their overall effect on the prognosis of the disease. The researchers conducted a systematic review following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines and collected data from several databases, including PubMed, PubMed Central, Cochrane Library, and Web of Science. The search strategy combined keywords related to CRC, COX-2 inhibitors, protective effects, and prognosis. They identified 1189 articles and shortlisted 26 full-text articles that met the eligibility criteria. Quality assessment tools, such as the Assessment of Multiple Systematic Review (AMSTAR) for systematic reviews, the Cochrane bias assessment tool for randomized control trials, the scale for the assessment of narrative review articles (SANRA) checklist for narrative reviews, and the Joanna Briggs Institute (JBI) tool for crosssectional studies and case reports, are used. This review's conclusions will assist in determining the effectiveness of COX-2 inhibitors to prevent CRC. This review may also contribute to developing guidelines for clinicians to manage genetically predisposed individuals with CRC. Furthermore, the results of this review will shed light on the potential of COX-2 inhibitors as a preventive measure against CRC in genetically predisposed individuals.

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Celecoxib as an adjuvant to chemotherapy for patients with metastatic colorectal cancer

Cited by 10 publications

References 30 publications

Peiyuan-Huayu Formula Suppresses Proliferation Migration and Angiogenesis of Human Microvascular Endothelial Cells-1 Through Activating MEK/ERK Signaling Pathway

Peiyuan-Huayu Formula Suppresses Proliferation Migration and Angiogenesis of Human Microvascular Endothelial Cells-1 Through Activating MEK/ERK Signaling Pathway

Role of myeloid-derived suppressor cells in tumor recurrence

Protective Effects of Long-Term Usage of Cyclo-Oxygenase-2 Inhibitors on Colorectal Cancer in Genetically Predisposed Individuals and Their Overall Effect on Prognosis: A Systematic Review

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