Downregulation of miR-375 contributes to ERBB2-mediated VEGFA overexpression in esophageal cancer

Ren, Shuchang; Tan, Xiaohui; Fu, Melinda Z.; Ren, Shuyang; Wu, Xiaoling; Chen, Tao; Latham, Patricia S.; Lin, Paul; Man, Yan‐gao; Fu, Sidney W.

doi:10.7150/jca.63836

Cited by 10 publications

(11 citation statements)

References 41 publications

(45 reference statements)

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“…58–61 VEGFA is highly expressed in EC cells and tumors and stimulates their survival, migration, metastasis, angiogenesis, growth, and metastasis. 62,63…”

Section: Discussionmentioning

confidence: 99%

“…58–61 The VEGF pathway stimulates various malignant behaviors of EC cells and tumors, such as growth, metastasis, and angiogenesis. 62,63…”

Section: Discussionmentioning

confidence: 99%

“…[58][59][60][61] VEGFA is highly expressed in EC cells and tumors and stimulates their survival, migration, metastasis, angiogenesis, growth, and metastasis. 62,63 The pathways by which FDY003 exerts anticancer effects are crucial mediators of EC carcinogenesis and progression. The ErbB, MAPK, p53, and PI3 K-Akt pathways are involved in the risk, tumor-node-metastasis (TNM) staging, lymph node and distant metastasis, tumor progression and development, tumor depth and invasion, tumor stage, and overall and diseasefree survival of patients with EC.…”

Section: Discussionmentioning

confidence: 99%

“…[58][59][60][61] The VEGF pathway stimulates various malignant behaviors of EC cells and tumors, such as growth, metastasis, and angiogenesis. 62,63 The chemical and herbal components of FDY003, uncovered from the network pharmacological elucidation, have been reported to exhibit anticancer activities against EC. Cm, genkwanin, and isorhamnetin repress the proliferation of EC cells.…”

Section: Discussionmentioning

confidence: 99%

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A Network Pharmacological Elucidation of the Systematic Treatment Activities and Mechanisms of the Herbal Drug FDY003 Against Esophageal Cancer

Lee¹,

Kang

Park³

et al. 2022

Natural Product Communications

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Despite accumulating evidence for the value of herbal drugs for cancer treatment, the mechanisms underlying their effects have not been fully elucidated in a systematic manner. In this study, we performed a network pharmacological analysis to elucidate the anti-esophageal cancer (EC) properties of the herbal drug FDY003, a mixture of Artemisia capillaris Thunberg (AcT), Cordyceps militaris (Linnaeus) Link (Cm), and Lonicera japonica Thunberg (LjT). FDY003 reduced human EC cell viability and increased the pharmacological effects of chemotherapeutic drugs. There were 15 active pharmacological chemicals targeting 61 EC-associated genes and proteins in FDY003. The FDY003 targets were key regulators of major oncogenic EC-associated signaling pathways, such as phosphoinositide 3-kinase (PI3K)-Akt, hypoxia-inducible factor (HIF)-1, mitogen-activated protein kinase (MAPK), tumor necrosis factor (TNF), p53, Janus kinase (JAK)-signal transducer and activator of transcription (STAT), erythroblastic leukemia viral oncogene homolog (ErbB), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B), and vascular endothelial growth factor (VEGF) cascades. These EC-associated genes, proteins, and pathways targeted by FDY003 determine the malignant behaviors of EC cells, including cell death, survival, division, proliferation, and growth. This network pharmacological analysis provides an integrative view of the mechanisms by which FDY003 contributes to EC treatment.

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“…58–61 VEGFA is highly expressed in EC cells and tumors and stimulates their survival, migration, metastasis, angiogenesis, growth, and metastasis. 62,63…”

Section: Discussionmentioning

confidence: 99%

“…58–61 The VEGF pathway stimulates various malignant behaviors of EC cells and tumors, such as growth, metastasis, and angiogenesis. 62,63…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

A Network Pharmacological Elucidation of the Systematic Treatment Activities and Mechanisms of the Herbal Drug FDY003 Against Esophageal Cancer

Lee¹,

Kang

Park³

et al. 2022

Natural Product Communications

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show abstract

“…VEGFA is not only important to endothelial cell survival but also helps circulating endothelial cells reach new blood vessels. This in turn can promote tumor growth and angiogenesis, and thus VEGFA expression may become a new tumor biomarker [ 72 , 73 ]. VEGFA also participates in the development of PTC [ 74 ].…”

Section: Discussionmentioning

confidence: 99%

Circular RNA Pvt1 oncogene (CircPVT1) promotes the progression of papillary thyroid carcinoma by activating the Wnt/β-catenin signaling pathway and modulating the ratio of microRNA-195 (miR-195) to vascular endothelial growth factor A (VEGFA) expression

Zeng¹,

Yuan²,

Zhou³

et al. 2021

Bioengineered

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Circular RNAs (circRNAs) have been reported to be involved in the progression of papillary thyroid carcinoma (PTC). However, the role of circular RNA Pvt1 oncogene ( circPVT1) in PTC has rarely been reported. In this study, we aimed to investigate the function and mechanism of circPVT1 in PTC. The expression level of circPVT1, miR-195 and VEGFA were determined by reverse transcription‑quantitative PCR (RT‑qPCR). Fisher’s exact test was used to analyze the correlation between circPVT1 expression and PTC clinical features. Cell Counting Kit-8 (CCK-8) and 5-Ethynyl-2ʹ-deoxyuridine (EdU) staining assay and transwell assay were conducted to evaluate the cell proliferation, migration and invasion ability. Dual-luciferase reporter and Western blot assay were conducted for evaluating the correlation between miR-195 and circPVT1 or VEGFA . The results of RT-PCR showed that the expression level of circPVT1 was significantly upregulated in PTC tissues and cell lines. After downregulating circPVT1 expression in PTC cells, the abilities of cell proliferation, migration, and invasion were obviously suppressed, and the Wnt/β-catenin signaling pathway was also repressed. Besides, miR-195 could both bind to PVT1 and VEGFA , while PVT1 could promote the expression of VEGFA by binding to miR-195 . Downregulation of VEGFA expression in PTC cells revealed weakened cell proliferation, migration, and invasion capacities, and restrained Wnt/β-catenin signaling pathway. Therefore, we demonstrated that circPVT1 could promote VEGFA expression by sponging miR-195. CircPVT1 could serve as a molecule sponge for miR-195 and mediate the ceRNA network to promote the expression of VEGFA , thus contributed to the malignant progression of PTC.

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MicroRNA‐299‐3p inhibits cell proliferation, motility, invasion and angiogenesis via VEGFA in upper tract urothelial carcinoma

Wang,

Lee,

Jhan

et al. 2023

The Journal of Gene Medicine

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BackgroundUpper tract urothelial carcinoma (UTUC) is a rare tumor with extraordinarily different features between Eastern and Western countries. Vascular endothelial growth factor‐A (VEGFA) was originally identified as a secreted signaling protein and regulator of vascular development and cancer progression. In this study, we aimed to elucidate the molecular mechanisms underlying the regulation of VEGFA by microRNA in UTUC.MethodsVEGFA expression was evaluated by immunohistochemistry in 140 human UTUC tissue samples. Next, we assessed the regulatory relationship between VEGFA and miR‐299‐3p by real‐time PCR, western blotting, ELISA and dual‐luciferase reporter assays using two UTUC cell lines. The role of miR‐299‐3p/VEGFA in cell proliferation, motility, invasion, and tube formation was analyzed in vitro.ResultsHigh VEGFA expression was significantly associated with tumor stage, grade, distant metastasis and cancer‐related death and correlated with poor progression‐free and cancer‐specific survival. VEGFA knockdown repressed proliferation, migration, invasion and angiogenesis in UTUC cell lines. miR‐299‐3p significantly reduced VEGFA protein expression and miR‐299‐3p overexpression inhibited VEGFA mRNA and protein expression by directly targeting its 3′‐UTR. Functional studies indicated that VEGFA overexpression reversed the miR‐299‐3p‐mediated suppression of tumor cell proliferation, migration, invasion and angiogenesis. In addition, miR‐299‐3p/VEGFA suppressed cellular functions in UTUC by modulating the expression of P18 and cyclin E2.ConclusionsOur findings suggest that miR‐299‐3p possibly suppresses UTUC cell proliferation, motility, invasion and angiogenesis via VEGFA. VEGFA may act as a prognostic predictor, and both VEGFA and miR‐299‐3p could be potential therapeutic targets for UTUC.

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Downregulation of miR-375 contributes to ERBB2-mediated VEGFA overexpression in esophageal cancer

Cited by 10 publications

References 41 publications

A Network Pharmacological Elucidation of the Systematic Treatment Activities and Mechanisms of the Herbal Drug FDY003 Against Esophageal Cancer

A Network Pharmacological Elucidation of the Systematic Treatment Activities and Mechanisms of the Herbal Drug FDY003 Against Esophageal Cancer

Circular RNA Pvt1 oncogene (CircPVT1) promotes the progression of papillary thyroid carcinoma by activating the Wnt/β-catenin signaling pathway and modulating the ratio of microRNA-195 (miR-195) to vascular endothelial growth factor A (VEGFA) expression

MicroRNA‐299‐3p inhibits cell proliferation, motility, invasion and angiogenesis via VEGFA in upper tract urothelial carcinoma

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