Salinomycin sensitizes antimitotic drugs-treated cancer cells by increasing apoptosis via the prevention of G2 arrest

Kim, Ju-Hwa; Yoo, Hye-In; Han, Kang; Ro, Jungsil; Yoon, Sungpil

doi:10.1016/j.bbrc.2011.12.141

Cited by 69 publications

(63 citation statements)

References 32 publications

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“…[15][16][17][18] Sal may also sensitize cancer cells to radiation or to cytostatic drugs, such as etoposide or doxorubicin, by increasing apoptosis as a result of enhancing DNA damage and reducing the levels of CDKN1A/p21 protein. [19][20][21] Evidence is emerging that Sal inhibits WNT-CTNNB1/β-catenin signaling by inducing WNT coreceptor lipoprotein receptor related protein 6 (LRP6) degradation. 22,23 In addition, Sal leads to an increase of cytosolic Ca 2+ through the Na + /Ca 2+ exchangers in the plasma membrane and mitochondria, and induces calpain and cytochrome c-mediated neuronal cell death.…”

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confidence: 99%

Inhibition of the autophagic flux by salinomycin in breast cancer stem-like/progenitor cells interferes with their maintenance

et al. 2013

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confidence: 99%

Inhibition of the autophagic flux by salinomycin in breast cancer stem-like/progenitor cells interferes with their maintenance

et al. 2013

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“…The impact of Salinomycin on human CC cells is reflected by cell cycle accumulation in the G2-phase. This finding is noticeable because others have demonstrated that treatment with Salinomycin in equal concentrations is associated with accumulation in the pre-G1-phase, indicating increased apoptosis [17] Furthermore, in pre-treated human breast cancer with antimitotic drugs, Salinomycin abolishes G2-arrest and aneuploid cell formation [17,40]. In contrast, radiationtreated breast cancer cells accumulate in the G2-phase after treatment with Salinomycin [41].…”

Section: Discussionmentioning

confidence: 97%

Impact of Salinomycin on human cholangiocarcinoma: induction of apoptosis and impairment of tumor cell proliferation in vitro

Lieke¹,

Ramackers²,

Bergmann³

et al. 2013

Z Gastroenterol

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Background: Cholangiocarcinoma (CC) is a primary liver cancer with increasing incidence worldwide. Despite all efforts made in past years, prognosis remains to be poor. At least in part, this might be explained by a pronounced resistance of CC cells to undergo apoptosis. Thus, new therapeutic strategies are imperatively required. In this study we investigated the effect of Salinomycin, a polyether ionophore antibiotic, on CC cells as an appropriate agent to treat CC. Salinomycin was quite recently identified to induce apoptosis in cancer stem cells and to overcome apoptosis-resistance in several leukemia-cells and other cancer cell lines of different origin. Methods: To delineate the effects of Salinomycin on CC, we established an in vitro cell culture model using three different human CC cell lines. After treatment apoptosis as well as migration and proliferation behavior was assessed and additional cell cycle analyses were performed by flowcytometry.

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“…It seems that several mechanisms of salinomycin action are currently discussed. 5,[17][18][19] Studies by Zhang et al in in vivo and in vitro conditions demonstrated that salinomycin induces apoptosis in the cells of ovarian cancer resistant to cisplatin, apoptosis linked to the pathway of mitogen-activated protein kinase (MAPK). 20 Studies by Kaplan and Teksen on the stable ovarian cancer cell line (OVCAR-3) demonstrated the activity of salinomycin: 40% of cells underwent apoptosis within 24 h of exposure.…”

Section: Salinomycinmentioning

confidence: 99%

Ovarian cancer stem cells: A target for oncological therapy

Markowska¹,

Sajdak²,

Huczyński³

et al. 2018

Adv Clin Exp Med

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According to numerous studies, failures in treatment of ovarian cancer, i.e., a relapse and metastases, result from a small population of cancer stem cells (CSCs). They may also be responsible for tumor initiation. Cancer stem cells are resistant to chemo-and radiotherapy. Eradication of CSCs may involve the application of salinomycin, metformin and Clostridium perfringens; the effect of anti-angiogenic factors remains controversial. Salinomycin is an antibiotic isolated from Streptomyces albus bacteria. Its CSC-eradicating effect has been demonstrated both in ovarian cancer cell lines and in women with breast cancer. Clostridium perfringens enterotoxin (CPE) has been demonstrated to destroy CSCs in ovarian cancer both in vivo and in vitro. Metformin, apart from its hypoglycemic effect, reduces the CSC population and inhibits the proliferation of neoplastic cells and angiogenesis. Cancer stem cells with expression of VEGFR1+ have been described as affecting circulating cancer cells and influencing the formation of metastases. Both positive and negative effects of anti-angiogenic therapy on the CSC population have been documented.

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Salinomycin sensitizes antimitotic drugs-treated cancer cells by increasing apoptosis via the prevention of G2 arrest

Cited by 69 publications

References 32 publications

Inhibition of the autophagic flux by salinomycin in breast cancer stem-like/progenitor cells interferes with their maintenance

Inhibition of the autophagic flux by salinomycin in breast cancer stem-like/progenitor cells interferes with their maintenance

Impact of Salinomycin on human cholangiocarcinoma: induction of apoptosis and impairment of tumor cell proliferation in vitro

Ovarian cancer stem cells: A target for oncological therapy

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