Genistein-induced differentiation of breast cancer stem/progenitor cells through a paracrine mechanism

Liu, Yanchen; Zou, Tong; Wang, Shuhuai; Chen, Hong; Su, Dongju; Fu, Xiaona; Zhang, Qingyuan; Kang, Xinmei

doi:10.3892/ijo.2016.3351

Cited by 33 publications

(28 citation statements)

References 48 publications

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“…Genistein inhibits tumorsphere formation, suppresses cell invasive capacity, and reduces chemoresistance in gastric cancer cells (Huang et al, ; Yu et al, ). Genistein decreases the population and induces differentiation of breast CSCs (Fan et al, ; Liu et al, ). However, the action of genistein on NCSCs has not been elucidated yet.…”

Section: Discussionmentioning

confidence: 99%

Genistein inhibits nasopharyngeal cancer stem cells through sonic hedgehog signaling

Zhang

Cao

Wang

et al. 2019

Phytotherapy Research

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Genistein, a soy derived isoflavanoid compound, exerts anticancer effects in various cancers. Nasopharyngeal cancer stem cells (NCSCs) are a small subpopulation of cancer cells which are responsible for initiation, progression, metastasis, and recurrence of nasopharyngeal cancer. The present study aimed to investigate the suppressive effects of genistein on NCSCs and its underlying mechanism. NCSCs were enriched from human nasopharyngeal cancer cell lines CNE2 and HONE1 through tumorsphere-forming assay. It was shown that genistein inhibited the tumorsphere formation capacity, decreased the number of EpCAM + cells, downregulated the expression of NCSCs markers, suppressed cell proliferation, and induced apoptosis of NCSCs. Genistein suppressed the activity of Sonic hedgehog (SHH) signaling, which was important for the maintenance of NCSCs, while activation of SHH signaling by purmorphamine diminished the inhibitory effects of genistein on NCSCs. Our data suggested that genistein inhibited NCSCs through the suppression of SHH signaling. These findings support the use of genistein for targeting NCSCs.

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Section: Discussionmentioning

confidence: 99%

Genistein inhibits nasopharyngeal cancer stem cells through sonic hedgehog signaling

Zhang

Cao

Wang

et al. 2019

Phytotherapy Research

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“…BC is one of the most common malignancies in women, and its incidence rate is the second highest in the world (18)(19)(20). Despite the existence of tumor stem cells in a variety of solid tumors and hematologic malignancies, there are presently many problems to be solved (21,22).…”

Section: Discussionmentioning

confidence: 99%

Involvement of breast cancer stem cells in tumor angiogenesis

Wang

et al. 2017

Oncol Lett

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Abstract. The aim of the present study was to investigate the role of breast cancer stem cells (BCSCs) in the angiogenesis of breast cancer tumors. The expression levels of mutant p53, cluster of differentiation (CD)31, vascular endothelial factor (VEGF), in addition to human epidermal growth factor (HER)2, were detected in the blood vessels of human breast cancer (BC) tissue samples. CD44 + /CD24 -/low cells were selected from single-cell suspensions of BC tissues to assess the expression of CD31 and CD105, in addition to the ability of these cells to metabolize acetylated low-density lipoprotein (Ac-LDL). Furthermore, vascular-like structures were observed histologically. Mutant p53, CD31 and VEGF were all expressed in these tissues. CD44+ cells comprised 7.5±2.6 and 94.3±4.7% of the cell population prior to and following sorting, respectively. CD24 + cells comprised 48.2±9.4 and 4.3±4% of the cell population prior to and following sorting, respectively. A low proportion of CD24 + cells corresponded to a high proportion of CD24 -/low cells. The percentages of CD105 + and CD31 + glomus cells in the mammary gland were 4.5±0.9 and 6.2±1.3%, respectively, and following passaging for three generations, these increased to 79.6±9.3 and 84.1±10.7%, respectively (P<0.05). Cells were cultured using an endothelial cell culture system, and they internalized DiL-Ac-LDL. Here, vascular endothelial cells formed vascular-like structures, whereas the control group demonstrated no such structures. Overall, the results suggest that BCSCs-derived endothelial cells may contribute to tumor angiogenesis.

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“…Numerous studies have reported that genistein abolishes stemness in CSCs or CSLCs via inhibition of AKT phosphorylation and activity (10,16). We thus hypothesized that the novel genistein analogue DFOG-inhibited spheroid and colony formation is associated with AKT inactivation.…”

Section: Dfog Reduces the Phosphorylation Levels Of Akt Inmentioning

confidence: 94%

Inactivation of AKT, ERK and NF-κB by genistein derivative, 7-difluoromethoxyl-5,4′-di-n-octylygenistein, reduces ovarian carcinoma oncogenicity

Ning

Cao

et al. 2017

Oncology Reports

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Abstract. Cancer stem cells (CSCs) have central functions in cancer formation and development. Aberrant expression of AKT, ERK and NF-κB signaling pathways have been reported in several types of CSCs. Phytochemicals from dietary compounds possess anti-CSC properties, and have been characterized as promising therapeutic agents for the prevention and treatment of many types of cancers. We previously showed that the newly synthesized genistein derivative, 7-difluoromethoxyl-5,4'-di-n-octylygenistein (DFOG), can inhibit the self-renewal ability of ovarian cancer stem cells (OVCSLCs). In the present study, we further assessed whether various signaling pathways are regulated by DFOG. We found that spheroids derived from the SKOV3 cell line possessed OVCSLC properties and DFOG efficiently inhibited the stemness of the OVCSLCs. In addition, the suppression of spheroid and colony formation by DFOG was associated with inhibition of AKT and ERK1/2 protein phosphorylation, and NF-κB activity in OVCSLCs from the SKOV3 cells. Importantly, DFOG inhibited the oncogenicity of the OVCSLCs by activation of FoxO3a and/or inactivation of FoxM1 by the targeting of multiple pro-survival (AKT and ERK1/2) and proinflammatory (NF-κB) pathways, providing a new avenue for the treatment of ovarian carcinoma in humans.

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Genistein-induced differentiation of breast cancer stem/progenitor cells through a paracrine mechanism

Cited by 33 publications

References 48 publications

Genistein inhibits nasopharyngeal cancer stem cells through sonic hedgehog signaling

Genistein inhibits nasopharyngeal cancer stem cells through sonic hedgehog signaling

Involvement of breast cancer stem cells in tumor angiogenesis

Inactivation of AKT, ERK and NF-κB by genistein derivative, 7-difluoromethoxyl-5,4′-di-n-octylygenistein, reduces ovarian carcinoma oncogenicity

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