RETRACTED ARTICLE: TGF-β secreted by tumor-associated macrophages promotes proliferation and invasion of colorectal cancer via miR-34a-VEGF axis

Zhang, Danhua; Qiu, Xinguang; Li, Jianhua; Zheng, Shusen; Liu, Liwen; Zhao, Hongchao

doi:10.1080/15384101.2018.1556064

Cited by 60 publications

(50 citation statements)

References 22 publications

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“…Rosano et al 28 revealed that miR-29a-3p can identify patients with colorectal cancer who are responding to anti-angiogenic therapy. Zhang et al 29 reported that miR-34a played an anti-tumor role by inhibiting the expression of VEGF in colorectal cancer. Double luciferase reporter assay revealed that miR-519d-3p could inhibit the fluorescence intensity of VEGF 3ʹ-UTR-wt vector significantly, but not VEGF 3ʹ-UTR-mut vector.…”

Section: Discussionmentioning

confidence: 99%

<p>miR-519d-3p Overexpression Inhibits P38 and PI3K/AKT Pathway via Targeting VEGFA to Attenuate the Malignant Biological Behavior of Non-Small Cell Lung Cancer</p>

Zhang

Yuan

et al. 2020

OTT

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Background: Non-small cell lung cancer (NSCLC) is a heterogeneous tumor that accounts for approximately 85% of all lung cancer cases worldwide. microRNAs (miRNAs) are believed to play an important role in regulating a variety of biological processes, including immunity and cancer. We investigated the effect of miR-519d-3p on the mitigation of NSCLC in vitro and in vivo. Methods: RT-PCR or immunohistochemical assays were used to assess the expression of miR-519d-3p. Colony formation, flow cytometry, and transwell assay were respectively used to detect proliferation, apoptosis, and invasion of A549 and NCI-H661 cell lines. Luciferase reporter assay was used to verify targeting the relationship between mir-519d-3p and VEGFA. Western blot was used to examine the expression of Ki67, caspase-3, E-cadherin, N-cadherin, VEGF, P38, and PI3K/AKT. Animal models were established by BABL/c mice to research the effect of mir-519d-3p overexpression in vivo. Results: In vitro, miR-519d-3p overexpression inhibited A549 and NCI-H661 cells proliferation, invasion, and also promoted apoptosis. In addition, miR-519d-3p overexpression downregulated VEGFA expression and decreased the P38 and PI3K/AKT phosphorylation level. In vivo, miR-519d-3p overexpression significantly restrained tumor volume (2087 ±265 mm 3 vs 599±135 mm 3 , *P< 0.05) and tumor weight (0.45±0.08 g vs 0.13±0.06 g, *P<0.05) compared with the control group. Overexpression of miR-519d-3p downregulated levels of Ki67 and N-cadherin significantly. Conclusion: The data indicated that miR-519d-3p could be a novel therapy or adjuvant against NSCLC.

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Section: Discussionmentioning

confidence: 99%

<p>miR-519d-3p Overexpression Inhibits P38 and PI3K/AKT Pathway via Targeting VEGFA to Attenuate the Malignant Biological Behavior of Non-Small Cell Lung Cancer</p>

Zhang

Yuan

et al. 2020

OTT

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“…TAMs are able to produce angiogenic factors, such as vascular endothelial growth factor (VEGF), platelet-derived growth factor and transforming growth factor β. TAMS also induce angiogenesis by expressing matrix metalloproteinase (MMPs) [27][28][29]. Angiogenesis inhibition therapy has recently become a promising therapeutic strategy for HCC.…”

Section: Tumor-associated Macrophagesmentioning

confidence: 99%

Current perspectives on the immunosuppressive tumor microenvironment in hepatocellular carcinoma: challenges and opportunities

et al. 2019

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Incidence of hepatocellular carcinoma (HCC) is on the rise due to the prevalence of chronic hepatitis and cirrhosis. Although there are surgical and chemotherapy treatment avenues the mortality rate of HCC remains high. Immunotherapy is currently the new frontier of cancer treatment and the immunobiology of HCC is emerging as an area for further exploration. The tumor microenvironment coexists and interacts with various immune cells to sustain the growth of HCC. Thus, immunosuppressive cells play an important role in the anti-tumor immune response. This review will discuss the current concepts of immunosuppressive cells, including tumor-associated macrophages, marrow-derived suppressor cells, tumor-associated neutrophils, cancer-associated fibroblasts, and regulatory T cell interactions to actively promote tumorigenesis. It further elaborates on current treatment modalities and future areas of exploration.

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“…VEGF, a potent angiogenic factor, serves a key role in the formation of new blood vessels in CRC (41). VEGF is upregulated in CRC tissues and anti-VEGF therapy has been applied to patients with metastatic CRC (42,43). A previous study demonstrated that CCAT1 downregulation decreased thyroid cancer cell viability, proliferation, migration and invasion, and reduced VEGF expression (44).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA CCAT1 promotes colorectal cancer cell migration, invasiveness and viability by upregulating VEGF via negative modulation of microRNA‑218

Zou

et al. 2020

Exp Ther Med

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Increasing evidence has demonstrated that long non-coding (lnc) RNA is aberrantly expressed in numerous types of cancer. Colorectal cancer is a common malignancy; however, the role and mechanism underlying the influence of lncRNA-colon cancer associated transcript 1 (CCAT1) in colorectal cancer is yet to be elucidated. The present study revealed that CCAT1 is highly expressed in colorectal cancer tissues. Bioinformatics analysis and a dual-luciferase reporter gene assay indicated that CCAT1 and microRNA (miR)-218 had complementary binding sites. Furthermore, reverse transcription-quantitative PCR revealed that miR-218 was downregulated in colorectal cancer tissues compared with paired adjacent healthy tissues. To investigate the biological effects of CCAT1 on colorectal cancer cells, MTT and Transwell assays were performed. The results revealed that when compared with the control group, CCAT1-short hairpin (sh)RNA significantly inhibited colorectal cancer cell (SW480) viability and decreased migration and invasiveness. In addition, CCAT1-shRNA significantly reduced vascular endothelial growth factor (VEGF) expression in SW480 cells; however, these effects were partially rescued by an miR-218 inhibitor. Furthermore, it was revealed that the CCAT1-plasmid significantly promoted the viability of SW480 cells, increased cell migration and invasiveness, and significantly increased VEGF expression. However, these effects were also partially rescued by with a miR-218 mimic. Taken together, the present results identified that the CCAT1/miR-218 axis serves a key role in the regulation of colorectal cancer progression, which may be used as potential therapeutic target for the treatment of colorectal cancer.

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RETRACTED ARTICLE: TGF-β secreted by tumor-associated macrophages promotes proliferation and invasion of colorectal cancer via miR-34a-VEGF axis

Cited by 60 publications

References 22 publications

<p>miR-519d-3p Overexpression Inhibits P38 and PI3K/AKT Pathway via Targeting VEGFA to Attenuate the Malignant Biological Behavior of Non-Small Cell Lung Cancer</p>

<p>miR-519d-3p Overexpression Inhibits P38 and PI3K/AKT Pathway via Targeting VEGFA to Attenuate the Malignant Biological Behavior of Non-Small Cell Lung Cancer</p>

Current perspectives on the immunosuppressive tumor microenvironment in hepatocellular carcinoma: challenges and opportunities

Long non‑coding RNA CCAT1 promotes colorectal cancer cell migration, invasiveness and viability by upregulating VEGF via negative modulation of microRNA‑218

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