Literature DB >> 28401486

Dual treatment with shikonin and temozolomide reduces glioblastoma tumor growth, migration and glial-to-mesenchymal transition.

Diana Matias1,2, Joana Balça-Silva1,3,4, Luiz Gustavo Dubois1, Bruno Pontes2, Valéria Pereira Ferrer1, Luciane Rosário1, Anália do Carmo3,5, Juliana Echevarria-Lima6, Ana Bela Sarmento-Ribeiro3,4,5, Maria Celeste Lopes3,7, Vivaldo Moura-Neto8.   

Abstract

PURPOSE: Glioblastomas (GBM) comprise 17% of all primary brain tumors. These tumors are extremely aggressive due to their infiltrative capacity and chemoresistance, with glial-to-mesenchymal transition (GMT) proteins playing a prominent role in tumor invasion. One compound that has recently been used to reduce the expression of these proteins is shikonin (SHK), a naphthoquinone with anti-tumor properties. Temozolomide (TMZ), the most commonly used chemotherapeutic agent in GBM treatment, has so far not been studied in combination with SHK. Here, we investigated the combined effects of these two drugs on the proliferation and motility of GBM-derived cells.
METHODS: The cytotoxic and proliferative effects of SHK and TMZ on human GBM-derived cells were tested using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), Ki67 staining and BrdU incorporation assays. The migration capacities of these cells were evaluated using a scratch wound assay. The expression levels of β3 integrin, metalloproteinases (MMPs) and GMT-associated proteins were determined by Western blotting and immunocytochemistry.
RESULTS: We found that GBM-derived cells treated with a combination of SHK and TMZ showed decreases in their proliferation and migration capacities. These decreases were followed by the suppression of GMT through a reduction of β3 integrin, MMP-2, MMP-9, Slug and vimentin expression via inactivation of PI3K/AKT signaling.
CONCLUSION: From our results we conclude that dual treatment with SHK and TMZ may constitute a powerful new tool for GBM treatment by reducing therapy resistance and tumor recurrence.

Entities:  

Keywords:  Glial-to-mesenchymal transition; Glioblastoma; Migration; Shikonin; Temozolomide

Mesh:

Substances:

Year:  2017        PMID: 28401486     DOI: 10.1007/s13402-017-0320-1

Source DB:  PubMed          Journal:  Cell Oncol (Dordr)        ISSN: 2211-3428            Impact factor:   6.730


  45 in total

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8.  Sensitizing the therapeutic efficacy of taxol with shikonin in human breast cancer cells.

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9.  Connective tissue growth factor (CTGF/CCN2) is negatively regulated during neuron-glioblastoma interaction.

Authors:  Luciana F Romão; Fabio A Mendes; Natalia M Feitosa; Jane Cristina O Faria; Juliana M Coelho-Aguiar; Jorge Marcondes de Souza; Vivaldo Moura Neto; José Garcia Abreu
Journal:  PLoS One       Date:  2013-01-31       Impact factor: 3.240

10.  Epithelial-mesenchymal transition in glioblastoma progression.

Authors:  Yasuo Iwadate
Journal:  Oncol Lett       Date:  2016-01-14       Impact factor: 2.967

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2.  QKI deficiency maintains glioma stem cell stemness by activating the SHH/GLI1 signaling pathway.

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10.  Inhibition of the STAT3 Signaling Pathway Contributes to the Anti-Melanoma Activities of Shikonin.

Authors:  Hui-Hui Cao; Dong-Yi Liu; Ye-Cai Lai; Yu-Yao Chen; Lin-Zhong Yu; Meng Shao; Jun-Shan Liu
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