MMP2/3 promote the growth and migration of laryngeal squamous cell carcinoma via PI3K/Akt‐NF‐κB‐mediated epithelial–mesenchymal transformation

Yunfen, Zhu; Li, Yan; Zhu, Wenjia; Song, Xinmao; Yang, Gang; Wang, Shengzi

doi:10.1002/jcp.28242

Cited by 39 publications

(26 citation statements)

References 22 publications

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“…Not only is hyperactivation of PI3K/AKT pathway in relation to NPC progression and prognosis [79], but FOXO1, CHL1, PNUTS, VPS33B interacts with NESG1, RBM3, ARHGAP42 and LncRNA ZFAS1 also display their influence on the proliferation, growth, invasion, metastasis, EMT, chemosensitivity or radio-resistance of NPC cells via PI3K/AKT pathway [93]. Additionally, MMP2/3, MEOX2, miR-145 and -138 regulate the growth, apoptosis or migration of LSCC cells by targeting the PI3K/AKT pathway [94][95][96][97].…”

Section: Characterization Of the Pi3k/akt Pathway In The Respiratory mentioning

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: Characterization Of the Pi3k/akt Pathway In The Respiratory mentioning

confidence: 99%

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

et al. 2020

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“…RAC1 is an important member of the small G protein Rho (Ras homologue) family. RAC1 binds to nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) enzymes and is involved in the production of intracellular reactive oxygen species (ROS) (Cadenas, 2018), regulating matrix metalloproteinase-3 (MMP-3) (Zhu et al, 2019). Activated RAC1 protein participates in the formation of actin stress fibers and adhesion plaques, promoting cytoskeleton reorganization (Grobe et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of chemotherapy-related breast tumor EMT by application of redox-sensitive siRNA delivery system CSO-ss-SA/siRNA along with doxorubicin treatment

Liu

Zhou

Shang

et al. 2020

J. Zhejiang Univ. Sci. B

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Metastasis is one of the main reasons causing death in cancer patients. It was reported that chemotherapy might induce metastasis. In order to uncover the mechanism of chemotherapy-induced metastasis and find solutions to inhibit treatment-induced metastasis, the relationship between epithelial-mesenchymal transition (EMT) and doxorubicin (DOX) treatment was investigated and a redox-sensitive small interfering RNA (siRNA) delivery system was designed. DOX-related reactive oxygen species (ROS) were found to be responsible for the invasiveness of tumor cells in vitro, causing enhanced EMT and cytoskeleton reconstruction regulated by Ras-related C3 botulinum toxin substrate 1 (RAC1). In order to decrease RAC1, a redox-sensitive glycolipid drug delivery system (chitosan-ss-stearylamine conjugate (CSO-ss-SA)) was designed to carry siRNA, forming a gene delivery system (CSO-ss-SA/siRNA) downregulating RAC1. CSO-ss-SA/siRNA exhibited an enhanced redox sensitivity compared to nonresponsive complexes in 10 mmol/L glutathione (GSH) and showed a significant safety. CSO-ss-SA/siRNA could effectively transmit siRNA into tumor cells, reducing the expression of RAC1 protein by 38.2% and decreasing the number of tumor-induced invasion cells by 42.5%. When combined with DOX, CSO-ss-SA/siRNA remarkably inhibited the chemotherapy-induced EMT in vivo and enhanced therapeutic efficiency. The present study indicates that RAC1 protein is a key regulator of chemotherapy-induced EMT and CSO-ss-SA/siRNA silencing RAC1 could efficiently decrease the tumor metastasis risk after chemotherapy.

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“…In the non-classical Smad signaling pathways, Xing et al (2018) found that 10 ng/mL TGF-b1 induced the EMT in hepatocellular carcinoma cells and that the PI3K/Akt/mTOR signaling pathway plays an important role in the EMT. Zhu et al (2019) found that matrix metalloproteinase (MMP) 2/3 overexpression in laryngeal squamous cell carcinoma promotes the EMT. More importantly, MMP2/3 promotes the development of laryngeal squamous cell carcinoma in a PI3K/Akt-NF-jB-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

NRP1 regulates radiation-induced EMT via TGF-β/Smad signaling in lung adenocarcinoma cells

Chen

Gao

Dong

et al. 2020

International Journal of Radiation Biology

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Purpose: Radiation has been shown to promote the epithelial-mesenchymal transition (EMT) in tumor cells, and TGF-b/Smad and PI3K-Akt signaling pathways play an important role in the EMT. In this study, we investigated the effects of neuropilin-1 (NRP1) on radiation-induced TGF-b/Smad and non-classical Smad signaling pathways in lung cancer cells, as well as the effects of NRP1 on invasion and migration. Materials and methods: Changes in the expression levels of EMT markers (b-catenin, N-cadherin, and vimentin) and related transcription factors (Twist and ZEB1) in stably transfected cells were detected by Western blotting and qPCR, and changes were assessed by TGF-b/Smad and non-classical Smad signaling. Immunofluorescence was used to detect the expression of the cytoskeletal protein F-actin. Expression of TGF-b1 and CXCL-12 was detected by ELISA. Transwell and scratch assays were used to detect the invasive ability and migration of lung cancer cells, respectively. Results: Our results showed that ionizing radiation could induce the EMT as well as morphological changes in lung adenocarcinoma cells (A549); however, the effects were not significant in lung squamous carcinoma cells (SK-MES-1). Moreover, we showed that NRP1 promotes the EMT induced by ionizing radiation in A549 cells, which may be related to the increased expression of EMT-related transcription factors. NRP1 may promote the radiation-induced EMT of A549 cells mainly through TGF-b1/Smad2/3 signaling. NRP1 also enhanced radiation-induced invasion, migration, and CXCL-12 expression in A549 cells. Conclusions: We conclude that NRP1 promotes radiation-induced EMT in lung adenocarcinoma cells via TGF-b1/Smad signaling and not non-classical Smad signaling, and enhances the invasion and migration of lung adenocarcinoma cells.

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MMP2/3 promote the growth and migration of laryngeal squamous cell carcinoma via PI3K/Akt‐NF‐κB‐mediated epithelial–mesenchymal transformation

Cited by 39 publications

References 22 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

Inhibition of chemotherapy-related breast tumor EMT by application of redox-sensitive siRNA delivery system CSO-ss-SA/siRNA along with doxorubicin treatment

NRP1 regulates radiation-induced EMT via TGF-β/Smad signaling in lung adenocarcinoma cells

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