Arctigenin inhibits triple-negative breast cancers by targeting CIP2A to reactivate protein phosphatase 2A

Huang, Qingqing; Qin, Shanshan; Yuan, Xianglin; Zhang, Liang; Ji, Juanli; Li, Xuewen; Ma, Wenjing; Zhang, Yunfei; Liu, Pengfei; Sun, Zhiting; Zhang, Jingxuan; Liu, Ying

doi:10.3892/or.2017.5667

Cited by 27 publications

(13 citation statements)

References 27 publications

(25 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…PP2A, a serine/threonine‐specific phosphatases of multiple oncogenic signaling proteins in cells, is down‐regulated in various cancer cells, and a promising therapeutic target for cancer treatment . Reactivation of PP2A can suppress many cancer cell proliferation and tumor growth . In our experiments, we found that knockdown of PP2A reversed the miR‐21 inhibitor‐induced osteosarcoma cell viability, migration, and invasion inhibition, which implied that ASBEL and miR‐21 promoted osteosarcoma cell viability, migration, and invasion by down‐regulation of PP2A.…”

Section: Discussionsupporting

confidence: 49%

Retracted: Long non‐coding RNA ASBEL promotes osteosarcoma cell proliferation, migration, and invasion by regulating microRNA‐21

Zhao

Zhang

Gao

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

Osteosarcoma is the most common malignant bone tumor in children and adolescents with high rate of incidence, high frequency of recurrence, and high degree of metastasis. This study aimed to investigate the effects of long noncoding RNA antisense ncRNA in the abundant in neuroepithelium area (ANA)/B-cell translocation gene 3 (BTG3) locus (lncRNA ASBEL) on the pathogenesis of osteosarcoma. The expression levels of ASBEL in human osteoblast cells and human osteosarcoma cells were evaluated using qRT-PCR. Effects of ASBEL knockdown on cell viability, migration, and invasion were detected using trypan blue exclusion assay, cell migration, and cell invasion assay, respectively. The regulatory effects of ASBEL on microRNA-21 (miR-21) were analyzed using qRT-PCR. The roles of miR-21 and protein phosphatase 2A (PP2A), the possible downstream factor of miR-21, in osteosarcoma cell proliferation, migration, and invasion were also explored. The results showed that ASBEL was highly expressed in osteosarcoma cells. Knockdown of ASBEL inhibited osteosarcoma cell viability, migration, and invasion, as well as the expression level of miR-21. PP2A was a direct target of miR-21, which participated in the effects of ASBEL and miR-21 on the activation of phosphatidylinositol 3-kinase/protein kinase 3/glycogen synthase kinase-3β (PI3K/AKT/GSK3β) and mitogen-activated protein kinase/extracellular regulated protein kinase (MEK/ERK) signaling pathways as well as the enhancement of osteosarcoma cell proliferation, migration, and invasion. In conclusion, we verified that ASBEL-miR-21-PP2A pathway might play critical regulatory effects on the pathogenesis of osteosarcoma and could be as the potential therapeutic target and biomarker for osteosarcoma treatment.

show abstract

Section: Discussionsupporting

confidence: 49%

Retracted: Long non‐coding RNA ASBEL promotes osteosarcoma cell proliferation, migration, and invasion by regulating microRNA‐21

Zhao

Zhang

Gao

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…This is consistent with the report that ATG increased cisplatin sensitivity in non-small cell lung cancer cells [21]. Furthermore, several studies showed that ATG suppresses chemical-induced metastatic potential in breast cancer cells, induces cell death of triple-negative breast cancer cells and has no significant toxicity less than 6 mg/kg in beagle dongs [20,65,66]. Anticancer drugs, such as doxorubicin, cisplatin, etc., have various side effects.…”

Section: Discussionsupporting

confidence: 90%

Arctigenin Enhances the Cytotoxic Effect of Doxorubicin in MDA-MB-231 Breast Cancer Cells

Lee

Kwon

et al. 2020

IJMS

View full text Add to dashboard Cite

Several reports have described the anti-cancer activity of arctigenin, a lignan extracted from Arctium lappa L. Here, we investigated the effect of arctigenin (ATG) on doxorubicin (DOX)-induced cell death using MDA-MB-231 human breast cancer cells. The results showed that DOX-induced cell death was enhanced by ATG/DOX co-treatment in a concentration-dependent manner and that this was associated with increased DOX uptake and the suppression of multidrug resistance-associated protein 1 (MRP1) gene expression in MDA-MB-231 cells. ATG enhanced DOX-induced DNA damage and decreased the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and the expressions of RAD51 and survivin. Cell death caused by ATG/DOX co-treatment was mediated by the nuclear translocation of apoptosis inducing factor (AIF), reductions in cellular and mitochondrial Bcl-2 and Bcl-xL, and increases in mitochondrial BAX levels. However, caspase-3 and -7 did not participate in DOX/ATG-induced cell death. We also found that DOX/ATG-induced cell death was linked with activation of the p38 signaling pathway and suppressions of the phosphorylations and expressions of Akt and c-Jun N-terminal kinase. Taken together, these results show that ATG enhances the cytotoxic activity of DOX in MDA-MB-231 human breast cancer cells by inducing prolonged p21 expression and p38-mediated AIF-dependent cell death. In conclusion, our findings suggest that ATG might alleviate the side effects and improve the therapeutic efficacy of DOX.

show abstract

“…Regarding the role of targeting CIP2A towards the treatment of breast cancer, the results of previous studies confirmed that Arctigenin inhibits triple-negative breast cancers proliferation, progression and invasion by targeting CIP2A to reactivate protein phosphatase 2A [48]. Moreover, CIP2A mediate bortezomib-induced apoptosis in TNBC cells.…”

Section: Discussionmentioning

confidence: 82%

Assessment of CIP2A and ROCK-I expression and their prognostic value in breast cancer

Osman¹,

Khalaf²,

Ibraheem³

2020

pjp

View full text Add to dashboard Cite

Breast cancer is the most leading cause of cancer death in females worldwide. Identification of novel biomarkers for prognosis is required. Imunohistochemical evaluation of CIP2A and ROCK-1 expressions in 126 breast tissue specimens stratified as 21 ductal hyperplasias, 17 duct carcinoma in situ (DCIS) and 88 invasive carcinomas (56 invasive ductal carcinomas NST, 32 invasive lobular carcinomas) was studied. High CIP2A expression was detected in 48.9% of invasive carcinomas. CIP2A overexpression was significantly related to Nottingham prognostic index (NPI) (p = 0.011), stage (p = 0.01), ER negativity (p = 0.031), PR negativity (p = 0.048), and HER-2 positivity (p = 0.02). CIP2A was significantly overexpressed in triple-negative breast cancer (TNBC) (p = 0.004). ROCK-1 expression was detected in 54.5% of invasive carcinomas. Statistically significant associations were observed between ROCK-1 expression and NPI (p = 0.032), stage (p = 0.002), ER negativity (p = 0.012), PR negativity (p = 0.023), HER-2 positivity (p = 0.016), and TNBC subtype (p = 0.033). A positive association between CIP2A and ROCK-1 expressions (p < 0.0001) was documented. There was a significant association between shorter overall survival and high CIP2A and positive ROCK-1 expressions (p < 0.0001) and (p < 0.0001). CIP2A and ROCK-1 expressions could be used as markers for the poor prognosis of breast cancer.

show abstract

Arctigenin inhibits triple-negative breast cancers by targeting CIP2A to reactivate protein phosphatase 2A

Cited by 27 publications

References 27 publications

Retracted: Long non‐coding RNA ASBEL promotes osteosarcoma cell proliferation, migration, and invasion by regulating microRNA‐21

Retracted: Long non‐coding RNA ASBEL promotes osteosarcoma cell proliferation, migration, and invasion by regulating microRNA‐21

Arctigenin Enhances the Cytotoxic Effect of Doxorubicin in MDA-MB-231 Breast Cancer Cells

Assessment of CIP2A and ROCK-I expression and their prognostic value in breast cancer

Contact Info

Product

Resources

About