MicroRNA‑433 inhibits cell growth and induces apoptosis in human cervical cancer through PI3K/AKT signaling by targeting FAK

Xu, Jie; Zhu, Weipei; Chen, Lijuan; Liu, Huan

doi:10.3892/or.2018.6718

Cited by 10 publications

(10 citation statements)

References 26 publications

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“…In particular, the mutations of PIK3CA E542K and E545K promote glycolysis and proliferation of CC in vitro and vivo [212]. NBPF1, ARHGAP17, miR-99b, -181a2/181b2, -338, -383, -433 and -489, as well as LncRNA ANRIL, CRNDE, NEAT1 and LINC01305 are involved in the proliferation, invasion, autophagy or EMT via PI3K/AKT pathway [213][214][215][216][217][218][219][220][221][222][223][224]. Currently, only preclinical trials of PI3K inhibitor LY294002 has revealed it significantly radiosensitized CC cell lines in vitro and vivo [225,226], and the terminated clinical trials of AKT inhibitor GSK2141795 (NCT01958112, Table 3) has tried to display a novel treatment approach to patients of CC.…”

Section: Nct02240212mentioning

confidence: 99%

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

et al. 2020

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Given that the PI3K/AKT pathway has manifested its compelling influence on multiple cellular process, we further review the roles of hyperactivation of PI3K/AKT pathway in various human cancers. We state the abnormalities of PI3K/AKT pathway in different cancers, which are closely related with tumorigenesis, proliferation, growth, apoptosis, invasion, metastasis, epithelial-mesenchymal transition, stem-like phenotype, immune microenvironment and drug resistance of cancer cells. In addition, we investigated the current clinical trials of inhibitors against PI3K/AKT pathway in cancers and found that the clinical efficacy of these inhibitors as monotherapy has so far been limited despite of the promising preclinical activity, which means combinations of targeted therapy may achieve better efficacies in cancers. In short, we hope to feature PI3K/ AKT pathway in cancers to the clinic and bring the new promising to patients for targeted therapies.

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Section: Nct02240212mentioning

confidence: 99%

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

et al. 2020

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“…In the same way, microRNA-433 induced the HeLa apoptosis via PI3K/AKT signal [32]. PI3K/AKT is involved in regulation cisplatin-resistance in cervical cancer [33].…”

Section: Discussionmentioning

confidence: 75%

S100A16 Regulates HeLa Cell through the Phosphatidylinositol 3 Kinase (PI3K)/AKT Signaling Pathway

Zhang

Yang

et al. 2020

Med Sci Monit

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Background: S100 calcium-binding protein A16 (S100A16) is closely related to the onset and progression of tumors. Material/Methods: In the research, the mainly purpose was to investigate the effect of S100A16 on the proliferation ability, invasion, and angiogenesis of HeLa cells. An adenoviral vector overexpressing S100A16 (Ad-S100A16) was constructed and transfected into HeLa cells, forming a stable cells line of overexpression. The effect of S100A16 on the proliferative capacity of HeLa cells was evaluated by a Cell Counting Kit-8 (CCK-8) assay. Cell migration capacity was determined by a Transwell migration assay. Changes in matrix metalloproteinase-2 (MMP-2), MMP-9, E-cadherin, and vimentin expression were evaluated by a cell-based immunofluorescence assay. The effect of S100A16 on angiogenesis was verified by knockout experiment. Results: Overexpression of S100A16 significantly enhanced the proliferative and migratory capacities of HeLa cells (P<0.05), upregulated expression of matrix MMP-2, MMP-9, vimentin, phosphatidylinositol 3 kinase, and phosphorylated protein kinase B, and downregulated expression of E-cadherin. Vascular endothelial growth factor expression increased, phosphatase and tensin homolog expression decreased, and angiogenesis was positively correlated with S100A16 expression. These effects were largely mediated by the activation of the phosphatidylinositol 3 kinase/protein kinase B pathways. Conclusions: S100A16 could promote the proliferation, migration, and tumor angiogenesis of HeLa cells by regulating the phosphatidylinositol 3 kinase/protein kinase B signaling pathways.

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“…77,78 Focal adhesion kinase (encoded by PTK2) suppresses apoptosis but promotes growth, proliferation, survival, EMT, tumorigenesis, migration, and invasion of CC cells and its expression is positively correlated with the progression, metastasis, angiogenesis, and the poor prognosis and clinical outcomes of patients with CC. [79][80][81][82][83][84][85][86] The expression and activity of TNF-α (encoded by TNF) is associated with the apoptosis, chemosensitivity, DNA damage response, necrosis, proliferation, invasion, and EMT of CC cells, and its polymorphisms are further correlated with the risk of development, progression, and malignancy in patients with CC. [87][88][89][90][91][92][93][94][95][96][97][98][99][100] The genetic or epigenetic malfunction of p53 (encoded by TP53), a key tumor suppressor that coordinates the cell cycle process, proliferation, apoptosis, DNA damage repair, and metabolism, can drive CC pathogenesis; therefore, the restoration of its expression or functional activity has been suggested as a potential strategy for treating CC.…”

Section: Discussionmentioning

confidence: 99%

“…109,111 Moreover, the complex interactions between these hub targets via various genetic and signaling mechanisms may modulate diverse CC-associated pathologic cellular processes, confer the pharmacological effects of anti-CC therapies, and contribute to the development of therapeutic resistance. 60,85,[112][113][114][115][116][117][118][119][120][121] Figure 2. Protein-protein interaction network for cervical cancer-associated targets of FDY2004.…”

Section: Discussionmentioning

confidence: 99%

A Comprehensive Understanding of the Anticancer Mechanisms of FDY2004 Against Cervical Cancer Based on Network Pharmacology

Lee¹,

Kang²,

Park³

et al. 2021

Natural Product Communications

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Herbal drugs are continuously being developed and used as effective therapeutics for various cancers, such as cervical cancer (CC); however, their mechanisms of action at a systemic level have not been explored fully. To study such mechanisms, we conducted a network pharmacological investigation of the anti-CC mechanisms of FDY2004, an herbal drug consisting of Moutan Radicis Cortex, Persicae Semen , and Rhei Radix et Rhizoma. We found that FDY2004 inhibited the viability of human CC cells. By performing pharmacokinetic evaluation and network analysis of the phytochemical components of FDY2004, we identified 29 bioactive components and their 116 CC-associated pharmacological targets. Gene ontology enrichment analysis showed that the modulation of cellular functions, such as apoptosis, growth, proliferation, and survival, might be mediated through the FDY2004 targets. The therapeutic targets were also key components of CC-associated oncogenic and tumor-suppressive pathways, including PI3K-Akt, human papillomavirus infection, IL-17, MAPK, TNF, focal adhesion, and viral carcinogenesis pathways. In conclusion, our data present a comprehensive insight for the mechanisms of the anti-CC properties of FDY2004.

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MicroRNA‑433 inhibits cell growth and induces apoptosis in human cervical cancer through PI3K/AKT signaling by targeting FAK

Cited by 10 publications

References 26 publications

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

Role of PI3K/AKT pathway in cancer: the framework of malignant behavior

S100A16 Regulates HeLa Cell through the Phosphatidylinositol 3 Kinase (PI3K)/AKT Signaling Pathway

A Comprehensive Understanding of the Anticancer Mechanisms of FDY2004 Against Cervical Cancer Based on Network Pharmacology

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