Epidermal growth factor receptor mutation enhances expression of vascular endothelial growth factor in lung cancer

Hung, Ming‐Szu; Chen, I‐Chuan; Lin, Paul‐Yann; Lung, Jrhau; Li, Ya‐Chin; Lin, Yu‐Ching; Yang, Cheng‐Ta; Tsai, Ying‐Huang

doi:10.3892/ol.2016.5287

Cited by 56 publications

(45 citation statements)

References 24 publications

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“…These results reinforce the notion that the miR-treatment correlates with a G 1 /S and G 2 /M inhibitor, albeit the mutational background of each cell line needs to be taken into consideration. Briefly, H358 cells carry a mutated KRAS and have an inactive (deleted) TP53 gene, while H1975 have a wt- KRAS , and mutated CDKN2A, PIK3CA, TP53 and EGFR genes ( 57 – 59 ). Our work compares and expands to our previously presented data on A549 cells, which carry wt- p53 , mutated KRAS and mutated CDKN2A .…”

Section: Discussionmentioning

confidence: 99%

Combination of miR‑143 and miR‑506 reduces lung and pancreatic cancer cell growth through the downregulation of cyclin‑dependent kinases

2021

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Lung cancer (LC) and pancreatic cancer (PC) are the first and fourth leading causes of cancer-related deaths in the US. Deregulated cell cycle progression is the cornerstone for rapid cell proliferation, tumor development, and progression. Here, we provide evidence that a novel combinatorial miR treatment inhibits cell cycle progression at two phase transitions, through their activity on the CDK4 and CDK1 genes. Following transfection with miR-143 and miR-506, we analyzed the differential gene expression of CDK4 and CDK1 , using qPCR or western blot analysis, and evaluated cell cycle inhibition, apoptosis and cytotoxicity. The combinatorial miR-143/506 treatment downregulated CDK4 and CDK1 levels, and induced apoptosis in LC cells, while sparing normal lung fibroblasts. Moreover, the combinatorial miR treatment demonstrated a comparable activity to clinically tested cell cycle inhibitors in inhibiting cell cycle progression, by presenting substantial inhibition at the G 1 /S and G 2 /M cell cycle transitions. More importantly, the miR-143/506 treatment presented a broader application, effectively downregulating CDK1 and CDK4 levels, and reducing cell growth in PC cells. These findings suggest that the miR-143/506 combination acts as a promising approach to inhibit cell cycle progression for cancer treatment with minimal toxicity to normal cells.

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Section: Discussionmentioning

confidence: 99%

Combination of miR‑143 and miR‑506 reduces lung and pancreatic cancer cell growth through the downregulation of cyclin‑dependent kinases

2021

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“…CSF3 (colony stimulating factor 3) is involved in various types of angiogenesis and skin wound healing by inducing VEGF release from neutrophils, thus promoting neovascularization ( 24 ). EGF (epidermal growth factor) is a member of the epidermal growth factor superfamily, which plays an important role in the growth, proliferation, and differentiation of numerous cell types, and has been demonstrated to have a critical role in tumor angiogenesis by enhancing the expression of VEGF ( 25 ). MMP1 (matrix metallopeptidase 1) has been identified as an important participant in tumor invasion, metastasis, and angiogenesis ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg3 targets cancer stem cells and tumor angiogenesis to inhibit colorectal cancer progression in vivo

et al. 2017

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Anti-angiogenic therapy has been successfully applied to treat colorectal cancer (CRC). Ginsenoside Rg3, derived from the Chinese herb ginseng, has anti-vascularization effects and can inhibit tumor growth and metastasis, and can sensitize cancer cells to chemotherapy. Therefore, in the present study, we investigated whether Rg3 could be appropriate for CRC treatment. Growth of CRC cells was assessed by an MTT (methyl thiazolyl tetrazolium) assay in vitro and using orthotopic xenograft models in vivo. mRNA expression was evaluated using real-time PCR. Protein levels were tested by western blotting, flow cytometry and immunohistochemistry. Migration was determined using a wound-healing assay. Stemness was further confirmed using a plate clone formation assay. We found that Rg3 repressed the growth and stemness of CRC cells both in vitro and in vivo. Rg3 also impaired the migration of CRC cells in vitro. Rg3 downregulated the expressions of angiogenesis-related genes, and repressed the vascularization of CRC xenografts. In addition, Rg3 strengthened the cytotoxicity of 5-Fluorouracil and oxaliplatin against orthotopic xenografts in vivo. Moreover, Rg3 downregulated the expressions of B7-H1 and B7-H3, high expressions of which were associated with reduced overall survival (OS) of CRC patients. Hence, Rg3 not only repressed the growth and stemness of CRC cells, but could also remodel the tumor microenvironment through repressing angiogenesis and promoting antitumor immunity. Therefore, Rg3 could be a novel therapeutic for the CRC treatment.

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“…37,38 Furthermore, in addition to being expressed on tumor cells, EGFR is also expressed on tumor-associated endothelial cells; therefore, it has been hypothesized that the dual inhibition of EGFR and VEGFR might yield greater antitumor activity. 39,40 VEGF can then promote tumor cell proliferation in an autocrine manner and enhance angiogenesis in a paracrine manner.…”

Section: Preclinical Evidence Of Dual Egfr-vegf Pathway Inhibition Inmentioning

confidence: 99%

Dual EGFR-VEGF Pathway Inhibition: A Promising Strategy for Patients With EGFR-Mutant NSCLC

Nilsson

Goldman

et al. 2021

Journal of Thoracic Oncology

187

120

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Blueprint, and Bayer; other fees from Altum Sequencing; and personal fees and other fees from Gernomica, Pharma Mar, and Ipsen outside of the submitted work. Ms. Frimodt-Moller is an employee of Eli Lilly and Company with stock holdings. Dr. Wolff is an employee of Eli Lilly and Company with stock holdings. Dr. Visseren-Grul is an employee of Eli Lilly and Company with stock holdings. Dr. Heymach has served on advisory committees

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Epidermal growth factor receptor mutation enhances expression of vascular endothelial growth factor in lung cancer

Cited by 56 publications

References 24 publications

Combination of miR‑143 and miR‑506 reduces lung and pancreatic cancer cell growth through the downregulation of cyclin‑dependent kinases

Combination of miR‑143 and miR‑506 reduces lung and pancreatic cancer cell growth through the downregulation of cyclin‑dependent kinases

Ginsenoside Rg3 targets cancer stem cells and tumor angiogenesis to inhibit colorectal cancer progression in vivo

Dual EGFR-VEGF Pathway Inhibition: A Promising Strategy for Patients With EGFR-Mutant NSCLC

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