Targeting CD151 by lentivirus-mediated RNA interference inhibits luminal and basal-like breast cancer cell growth and invasion

Liu, Ting; Wang, Shaoqing; Wang, Liping; Wang, Junping; Li, Yulin

doi:10.1007/s11010-015-2459-2

Cited by 15 publications

(10 citation statements)

References 32 publications

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“…In order to explore the effects of SIX1 knockdown on the proliferation capacity, we analyzed shSIX1-SNU398 and control-SNU398 HCC cell clones cell proliferation by MTT assay. Our results from cell viability assays were in line with previous studies [23,24], demonstrating that cellular proliferation is signi cantly inhibited in shSIX1-SNU398 at 24, 36 and 48 hours compared to control-SNU398 cells (Fig. 2d) Knockdown of SIX1 expression affects the expression levels of EMT markers Subsequently, the effect of SIX1 knockdown on ZEB1, ZEB2, TWIST, EPCAM, VIM, CDH1, SOX2, ITGA5 and ITGB1 expression levels was analyzed using RT-qPCR.…”

Section: Six1 Expression Levels Are Upregulated In Various Types Of Cancersupporting

confidence: 89%

SIX1 Down-Regulation Influence Drug Resistance, Epithelial-Mesenchymal Transcription Factors and Self-Renewal Capacity in Hepatocellular Carcinoma

Aysan

Salık

et al. 2021

Preprint

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Sine oculis homeoprotein 1 (SIX1) was discovered to exert an essential role in embryonic development and it was also identified to be re-activated in various types of mammalian cancer. Immunohistochemical and SIX1 gene expression analyses were performed to determine the prognostic role of SIX1 expression. SIX1 expression was suppressed by short hairpin RNA transduction in the SNU398 HCC cell line. The effects of SIX1 on proliferation, epithelial-mesenchymal transition, apoptosis, drug resistance, and sphere formation were assessed in SIX1 knock-down cells. The upregulated expression levels of SIX1 were revealed to be correlated with the stage of the disease in breast, colon and liver cancer, with liver cancer exhibiting the highest expression profile. SIX1 knockdown significantly affected the cell morphology, proliferation, downregulated the protein expression levels of ZEB1, ZEB2 and SNAI1 and upregulated the expression levels of TWIST1 in hepatocellular carcinoma cells. Furthermore, SIX1 knockdown cells were more sensitive to sorafenib treatment; however, the expression profile analysis of the drug resistance genes ABCB1, ABCC1 and ABCG2 did not explain this sensitivity. Finally, SIX1 knockdown cells were identified to have decreased CD90 levels and lost their sphere-forming ability, which is essential for cancer stem cell properties. Overall, these results indicated that SIX1 expression may be useful as a diagnostic marker for patients with HCC.

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Section: Six1 Expression Levels Are Upregulated In Various Types Of Cancersupporting

confidence: 89%

SIX1 Down-Regulation Influence Drug Resistance, Epithelial-Mesenchymal Transcription Factors and Self-Renewal Capacity in Hepatocellular Carcinoma

Aysan

Salık

et al. 2021

Preprint

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“…Increased Six1 was found to be associated with the poor prognosis of prostate cancer patients and enhanced pancreatic cancer cell proliferation through upregulation of cyclin D1 (28,29). Conversely, downregulation of Six1 suppressed colorectal cancer cell growth and invasion (30). From our results, we could infer that elevated HDAC5 could promote the expression of Six1 in lung cancer, and contribute to lung cancer cell proliferation and poor prognosis.…”

Section: Discussionmentioning

confidence: 55%

Histone deacetylase�5 promotes the proliferation and invasion of lung cancer cells

et al. 2018

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Histone deacetylase 5 (HDAC5), as a member of the class IIa family of HDACs, is frequently dysregulated in human malignancies. However, little is known regarding the specific role of HDAC5 in lung cancer. We aimed to evaluate HDAC5 expression in human lung cancer and to determine the effects of HDAC5 on lung cancer cells. First, the expression levels of both HDAC5 protein and mRNA were evaluated in lung cancer tissues and cell lines by western blot analysis and RT‑qPCR, and the results suggested that HDAC5 was significantly upregulated in human lung cancer tissues and cell lines. To address the effects of HDAC5 on the biological behavior of human lung adenocarcinoma cells, we generated human lung cancer A549 cell lines in which HDAC5 was either overexpressed or depleted. The results indicated that overexpression of HDAC5 significantly promoted the proliferation and invasion, and inhibited the apoptosis of A549 cells. On the contrary, HDAC5 knockdown largely decreased the proliferation and invasion and enhanced the apoptosis of A549 cells. Furthermore, we demonstrated that HDAC5 overexpression promoted the expression of DLL4, Six1, Notch 1 and Twist 1 in A549 cells. Downregulation of HDAC5 caused a significant inhibition of the expression of DLL4, Six1, Notch 1 and Twist 1 in A549 cells. Taken together, our data demonstrated that HDAC5 displayed a significant upregulation in lung cancer, and elevated HDAC5 might be involved in the potentiation of proliferation and invasion of lung cancer cells, as well as the inhibition of lung cancer cell apoptosis by the upregulation of DLL4, Six1, Notch 1 and Twist 1. The present study may provide an evidence for the potential application of HDAC5 inhibitors in the therapy of lung cancer.

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“…Lentiviral production, titration, and infection were performed as Li et al. described . Lentiviral plasmids pGMLV‐SC5 expressing shMALAT1 or control was cotransfected with the packaging vectors psPAX2 and pMD2.G into 293T cells using HG transgene reagent (Genomeditech, China).…”

Section: Methodsmentioning

confidence: 99%

Long noncoding RNA MALAT1 knockdown reverses chemoresistance to temozolomide via promoting microRNA‐101 in glioblastoma

2018

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Glioblastoma (GBM) is the most common and lethal tumor of the central nervous system with highly infiltrative and resistant to chemotherapy. Temozolomide (TMZ) is widely used as the first‐line treatment for the therapy of GBM. However, a considerable percentage inherent or acquired resistance in GBM accounts for many treatment failures of the TMZ chemotherapy. Therefore, a deeper understanding of the molecular characteristics underlying TMZ resistance and the identification of novel therapeutic target is urgent. Here, we show that MALAT1 was significantly upregulated in TMZ‐resistant GBM cells. On the other hand, MALAT1 knockdown reduces TMZ resistance of GBM cells both in vitro and in vivo by inhibiting cell proliferation and promoting apoptosis. We also show that miR‐101 overexpression reduced TMZ resistance of GBM cells and played an antagonistic role compared with MALAT1. Importantly, we demonstrate that MALAT1 promoted the chemoresistance through suppressing miR‐101 signaling pathway via directly binding it in GBM cells. In conclusion, our study indicates that knockdown of MALAT1 reverses chemoresistance to TMZ via promoting miR‐101 regulatory network in GBM and thus offers a novel prognostic marker and potential target for GBM TMZ‐based chemotherapy.

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Targeting CD151 by lentivirus-mediated RNA interference inhibits luminal and basal-like breast cancer cell growth and invasion

Cited by 15 publications

References 32 publications

SIX1 Down-Regulation Influence Drug Resistance, Epithelial-Mesenchymal Transcription Factors and Self-Renewal Capacity in Hepatocellular Carcinoma

SIX1 Down-Regulation Influence Drug Resistance, Epithelial-Mesenchymal Transcription Factors and Self-Renewal Capacity in Hepatocellular Carcinoma

Histone deacetylase�5 promotes the proliferation and invasion of lung cancer cells

Long noncoding RNA MALAT1 knockdown reverses chemoresistance to temozolomide via promoting microRNA‐101 in glioblastoma

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