Proscillaridin A is cytotoxic for glioblastoma cell lines and controls tumor xenograft growth in vivo

In our study, we explored the effect of AgIV on carboplatin chemotherapy in prostate cancer cell lines in vitro and in vivo. Cell viability assay, colony formation assay, flow cytometry, western blot, immunohistochemistry (IHC), immunofluorescence and tumor xenograft growth assay were conducted. We found that AgIV significantly decreased the half maximal inhibitory concentration (IC50) of carboplatin in prostate cancer cell lines LNCap and PC-3. Moreover, AgIV enhanced the effect of carboplatin in suppressing colony formation and inducing cell apoptosis. A low dose carboplatin treatment upregulated N-cadherin and Vimentin expression and downregulated E-cadherin expression, but this effect was abolished by combining with AgIV. Carboplatin treatment increased the levels of p-AKT and p-p65 and decreased p-IκBα, but AgIV treatment suppressed this. In addition, AgIV synergized with carboplatin to suppress tumor xenograft growth of PC-3 cells, and decreased pAKT and p-p65 levels in vivo. In summary, our results suggested that AgIV enhanced carboplatin sensitivity in prostate cancer cell lines by suppressing AKT/NF-кB signaling, thus suppressed EMT induced by carboplatin. Our findings provided a new mechanism for AgIV in overcoming drug resistance of platinum-based chemotherapy, and suggested a potential combination therapy of AgIV and carboplatin in prostate cancer.

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Effect of six retinoids and retinoic acid catabolic inhibitor liarozole on two glioblastoma cell lines, and in-vivo experience in malignant brain tumor patients

Cancer Treatment An Update ◽

10.1007/978-2-8178-0765-2_126 ◽

1994 ◽

pp. 590-598 ◽

Cited By ~ 1

Author(s):

M. E. Westarp ◽

M. P. Westarp ◽

W. Bollag ◽

J. Bruynseels ◽

H. Biesalski ◽

...

Keyword(s):

Brain Tumor ◽

Retinoic Acid ◽

Cell Lines ◽

Malignant Brain Tumor ◽

Glioblastoma Cell ◽

Tumor Patients ◽

Glioblastoma Cell Lines

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Circular RNA CDR1as Exerts Oncogenic Properties Partially through Regulating MicroRNA 641 in Cholangiocarcinoma

Molecular and Cellular Biology ◽

10.1128/mcb.00042-20 ◽

2020 ◽

Vol 40 (15) ◽

Cited By ~ 1

Author(s):

Dingyang Li ◽

Zhe Tang ◽

Zhiqiang Gao ◽

Pengcheng Shen ◽

Zhaochen Liu ◽

...

Keyword(s):

Cell Proliferation ◽

Target Genes ◽

Circular Rna ◽

Tumor Xenograft ◽

Mrna Levels ◽

Cell Behaviors ◽

Xenograft Growth ◽

Tumor Xenograft Growth

ABSTRACT It has been found that the circular RNA (circRNA) CDR1as is upregulated in cholangiocarcinoma (CCA) tissues. In this study, we tried to explore the roles of CDR1as in CCA. CDR1as was overexpressed or knocked down in human CCA cells to assess the effects of CDR1as on cell behaviors and tumor xenograft growth. In vitro, the CDR1as level was significantly increased in CCA cell lines. The results showed that CDR1as promoted the cell proliferation, migration, invasion, and activation of the AKT3/mTOR pathway in CCA cells. Moreover, miR-641, a predicted target microRNA (miRNA) of CDR1as, could partially reverse the effects of CDR1as on cell behaviors in CCA cells. Furthermore, CDR1as improved tumor xenograft growth, and it could be attenuated by miR-641 in vivo. Additionally, CDR1as expression was inversely correlated with miR-641 in CCA cells, and miR-641 could directly bind with CDR1as and its target genes, the AKT3 and mTOR genes. Mechanistically, CDR1as could bind with miR-641 and accelerate miR-641 degradation, which possibly leads to the upregulation of the relative mRNA levels of AKT3 and mTOR in RBE cells. In conclusion, our findings indicated that CDR1as might exert oncogenic properties, at least partially, by regulating miR-641 in CCA. CDR1as and miR-641 could be considered therapeutic targets for CCA.

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