ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014
Molecular regulation of cervical cancer growth and invasion by VEGFa.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Elucidating the tumor microenvironment interactions in breast, cervical, and ovarian cancer through single-cell RNA sequencing.Scientific reports · 2025Article
- Design, Synthesis, and Anti-Cervical Cancer and Reversal of Tumor Multidrug Resistance Activity of Novel Nitrogen-Containing Heterocyclic Chalcone Derivatives.Molecules (Basel, Switzerland) · 2023Article
- Article
- Identifying the critical state of complex biological systems by the directed-network rank score method.Bioinformatics (Oxford, England) · 2022Article
- Long non-coding RNA HAND2-AS1 delays cervical cancer progression via its regulation on the microRNA-21-5p/TIMP3/VEGFA axis.Cancer gene therapy · 2021Article
- Article
- Mechanism of Hedyotis Diffusa in the Treatment of Cervical Cancer.Frontiers in pharmacology · 2021Article
- The Communication Between the PI3K/AKT/mTOR Pathway and Y-box Binding Protein-1 in Gynecological Cancer.Cancers · 2020Review
- Inhibition of VEGFA Increases the Sensitivity of Ovarian Cancer Cells to Chemotherapy by Suppressing VEGFA-Mediated Autophagy.OncoTargets and therapy · 2020Article
- CKD-602, a topoisomerase I inhibitor, induces apoptosis and cell-cycle arrest and inhibits invasion in cervical cancer.Molecular medicine (Cambridge, Mass.) · 2019Article
- Identification of key genes and long non‑coding RNAs in celecoxib‑treated lung squamous cell carcinoma cell line by RNA‑sequencing.Molecular medicine reports · 2018Article
- The role of miR-106p-5p in cervical cancer: from expression to molecular mechanism.Cell death discovery · 2018Article
- Apatinib, a novel tyrosine kinase inhibitor, suppresses tumor growth in cervical cancer and synergizes with Paclitaxel.Cell cycle (Georgetown, Tex.) · 2018Article
- Adipocyte-derived exosomes promote lung cancer metastasis by increasing MMP9 activity via transferring MMP3 to lung cancer cells.Oncotarget · 2017Article
- YT521 promotes metastases of endometrial cancer by differential splicing of vascular endothelial growth factor A.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Pituitary tumor-transforming gene 1 enhances metastases of cervical cancer cells through miR-3666-regulated ZEB1.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- MiRNA-494 inhibits metastasis of cervical cancer through Pttg1.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Network Topologies Decoding Cervical Cancer.PloS one · 2015Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although antivascular endothelial growth factor a (VEGFa) treatment has been well applied in cervical cancer therapy, the underlying molecular basis has not been precisely identified. Here, we examined the levels of VEGFa on the tumor growth and invasion in four commonly used human cervical cancer cell lines. We found that overexpression of VEGFa in these lines increased the tumor growth and invasiveness, while inhibition of VEGFa decreased the tumor growth and invasiveness. To figure out the involved signaling pathways, we applied specific inhibitors for ERK/MAPK, JNK, and PI3K/Akt signaling pathways, respectively, to VEGFa-overexpressing cervical cancer lines and found that only inhibition of PI3K/Akt signal transduction abolished VEGFa-induced increases in cell growth and invasiveness. Inhibition of Akt downstream mTor signaling similarly inhibited cell growth and invasion in VEGFa-overexpressing cervical cancer cells, suggesting that VEGFa may activate PI3K/Akt, and subsequently its downstream mTor signaling pathway, to promote cervical cancer cell growth and invasion. Furthermore, the effects of VEGFa-induced activation of mTor signaling cascades appeared to promote cancer cell growth through cyclinD1 and CDK4 activation and promote cancer cell invasion through MMP2 and MMP3. Taken together, our data suggest that anti-VEGFa treatment in cervical cancer may inhibit both tumor cell growth and invasion through PI3k/Akt/mTor signaling pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.