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PYK2 mediates the BRAF inhibitor (vermurafenib)-induced invadopodia formation and metastasis in melanomas

Cancer Biology & Medicine 2022年第8期19卷 1211-1223页

作者： Junling Shen Jilong Yang Lei Sang Rui Sun Weiyu Bai Chao Wang Yan Sun Jianwei Sun Center for Life Sciences School of Life SciencesState Key Laboratory for Conservation and Utilization of Bio-Resources in YunnanYunnan UniversityKunming 650091China Tianjin Medical University Cancer Institute and Hospital National Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjin’s Clinical Research Center for CancerTianjinChina

Objective:The BRAF inhibitor,vemurafenib,has been widely used in the treatment of patients with melanoma-bearing BRAFV600E *** the initial response to vemurafenib is usually excellent,the majority of patients eventually develop resistance and metastatic ***,the underlying molecular mechanism remains *** objective of this study was therefore to identify additional molecular targets responsible for vemurafenib ***:Western blots and immunohistochemistry analyses were used to evaluate expressions of PYK2 and p-PYK2 in cultured cells and melanoma tissue *** relationships of p-PYK2 with clinicopathological parameters were statistically *** cell invasion,and a Ca2+assay were used to determine the effect of vemurafenib resistance-induced p-PYK2 on melanoma progression.A mouse model was used to assess the effects of PYK2 on melanoma ***:Elevated p-PYK2 levels were detected in vemurafenib-resistant melanoma cells,and PYK2 was shown to regulate invadopodia formation in melanoma *** triggered invadopodia formation by activation of *** of PYK2 with either shRNA or the small molecule inhibitor,PF562711,dramatically reduced vemurafenib-induced invadopodia ***,knockdown of PYK2 significantly reduced melanoma lung metastasis in *** expressions of p-PYK2 in melanoma patients were positively correlated with advanced stage(P=0.002),metastasis(P<0.001),and Clark grade(P<0.001),and were also associated with short overall survival[hazard ratio(HR)=3.304,P=0.007]and progression-free survival(HR=2.930,P=0.001).Conclusions:PYK2 mediated vemurafenib-induced melanoma cell migration and *** of PYK2 resensitized melanoma cells to ***-PYK2 was a prognostic biomarker in melanoma patients.

关键词： STIM1 Pyk2 invadopodia invasion melanoma vemurafenib

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Isotoosendanin exerts inhibition on triple-negative breast cancer through abrogating TGF-β-induced epithelial—mesenchymal transition via directly targeting TGFβR1

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药学学报:英文版 2023年第7期13卷 2990-3007页

作者： Jingnan Zhang Ze Zhang Zhenlin Huang Manlin Li Fan Yang Zeqi Wu Qian Guo Xiyu Mei Bin Lu Changhong Wang Zhengtao Wang Lili Ji The MOE Key Laboratory for Standardization of Chinese Medicines Shanghai Key Laboratory of Compound Chinese Medicines and the SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese MedicinesInstitute of Chinese Materia MedicaShanghai University of Traditional Chinese MedicineShanghai 201203China

As the most aggressive breast cancer,triple-negative breast cancer(TNBC) is still incurable and very prone to *** transform growth factor β(TGF-β)-induced epithelial—mesenchymal transition(EMT) is crucially involved in the growth and metastasis of *** study reported that a natural compound isotoosendanin(ITSN) reduced TNBC metastasis by inhibiting TGF-β-induced EMT and the formation of *** can directly interact with TGF-β receptor type-1(TGFβR1) and abrogated the kinase activity of TGFβR1,thereby blocking the TGF-β-initiated downstream signaling ***,the ITSN-provided inhibition on metastasis obviously disappeared in TGFβR1-overexpressed TNBC cells in vitro as well as in mice bearing TNBC cells overexpressed TGFβ***,Lys232 and Asp351 residues in the kinase domain of TGFβR1 were found to be crucial for the interaction of ITSN with TGFβ***,ITSN also improved the inhibitory efficacy of programmed cell death 1 ligand 1(PD-L1) antibody for TNBC in vivo via inhibiting the TGF-β-mediated EMT in the tumor *** findings not only highlight the key role of TGFβR1 in TNBC metastasis,but also provide a leading compound targeting TGFβR1 for the treatment of TNBC ***,this study also points out a potential strategy for TNBC treatment by using the combined application of anti-PD-L1 with a TGFβR1 inhibitor.

关键词： TNBC Isotoosendanin Metastasis TGFβR1 Epithelial-mesenchymal transition invadopodia PD-L1 Tumor microenvironment

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Compressive Stress Enhances Invasive Phenotype of Cancer Cells via Piezo1 Activation

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医用生物力学 2019年第A1期34卷 125-126页

作者： Mingzhi Luo Kenneth KYHo Zhaowen Tong Linhong Deng Allen PLiu Institute of Biomedical Engineering and Health Sciences Changzhou UniversityChangzhouJiangsuChina Department of Mechanical Engineering University of MichiganAnn ArborMichiganUSA Department of Biophysics University of MichiganAnn ArborMichiganUSA Department of Biomedical Engineering University of MichiganAnnArborMichiganUSA Cellular and Molecular Biology Program University of MichiganAnn ArborMichiganUSA

In this study,we hypothesized that Piezo 1 channels mediate the compression-enhanced invasive phenotype of cancer cells via a caveolae-dependent *** test this hypothesis,we examined in vitro cultured human breast cancer cells for their ability to invade and degrade extracellular matrix in the presence or absence of compressive stress,together with corresponding changes in Piezo1 as well as cytoskeletal remodeling and calcium *** we show that compressive stress enhanced invasion,matrix degradation,and invadopodia formation of breast cancer *** further identified Piezo1 as the putative mechanosensitive cellular component that transmits compression to induce calcium influx,which in turn triggers several downstream ***,for the first time we observed inv-adopodia with matrix degradation ability on the apical side of the cells, similar to those commonly observed at the cell s ventral ***,we demonstrate that Piezo1 and caveolae were both involved in mediating the compressive stress-induced cancer cell invasive phenotype as Piezo 1 and caveolae were often colocalized,and reduction of Cav-1 expression or disruption of caveolae with methyl-β-cyclodextrin led to not only reduced Piezo1 expression but also attenuation of the invasive phenotypes promoted by compressive *** together,we first observed that in breast cancer cells,simulating uncontrolled growth-induced compressive stress enhanced cancer cell invasion,matrix degradation,and invadopodia and stress fiber *** study also confirmed that Piezo1 channels are highly expressed in breast cancer cells compared to normal breast cells,and is consistent with the data that compressive stress regulates cell migration of breast cancer cells but not normal breast ***,we identified that Piezol mediated these processes and the invasive phenotypes also depended on the integrity of *** findings provide the first demonstration that compres

关键词： compressive stress caveolae Piezo1 invadopodia mechanotransduction

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Research on the Solution of Cell Invasion Model with Free Boundary

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Open Journal of Applied Sciences 2017年第6期7卷 242-261页

作者： Rouzimaimaiti Mahemuti Ahmadjan Muhammadhaji Takashi Suzuki College of Mathematics and System Sciences Xinjiang University Urumqi China Graduate School of Engineering Science Osaka University Osaka Japan

There are many works (i.e. [1]) aiming to find out numerically how positive feedback affects the formation of invadopodia and invasion of cancer cells;however, studies on the cancer cell invasion model with free boundary are fairly rare. In this paper, we study modified cancer cell invasion model with free boundary, where, free boundary stands for cancer cell membrane, so that we can more precisely describe the positive feedback affects. Firstly, we simplized the model by means of characteristic curve and semi-groups’ property, and obtained the Stefan-like problem by introducing Gaussian Kernel and Green function. Secondly, based on the classical Stefan problem, we derived the integral solution of simplified model, which could lead us a further step to find the solution of modified cancer cell invasion model.

关键词： invadopodia Cancer Stefan Problem Free Boundary

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Myosin 10 is necessary for breast cancer cell invasive growth and metastasis

Myosin 10 is necessary for breast cancer cell invasive growt...

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细胞—生命的基础——中国细胞生物学学会2013年全国学...

作者： Rangjuan Cao Jingying Chen Wanying Xing Lirong Zhang Huali Yu Xiaojuan Zhu School of Life Science Northeast Normal University China Japan Union Hospital of Jilin University

invadopodia are specialized actin-based membrane protrusions formed on the ventral surface of invasive cancer cells,and play a key role in ECM degradation and cancer cell *** 10 (Myo 10),a molecular motor,exhibits a striking localization at the tip of filopodia essential for many cell *** has reported that Myo 10 expression was higher in p53 mutants primary breast tumors

关键词： Myosin10 invadopodia metastasis PI3K

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