Salinomycin overcomes acquired tamoxifen resistance through <i><scp>AIB</scp>1</i> and inhibits cancer cell invasion in endocrine resistant breast cancer

Manmuan, Suwisit; Sakunrangsit, Nithidol; Ketchart, Wannarasmi

doi:10.1111/1440-1681.12806

Cited by 10 publications

(5 citation statements)

References 54 publications

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“…Meanwhile, some cell lines that were sensitive to Sal were not sensitive to the clinical commonly used drug cisplatin, including M29, SK-Mel-19, and A375 cell line (Supplementary Table S2 ). Some studies have indicated that Sal can specially damage tumor cells that are insensitive to drugs induced apoptosis, including drug resistant cancer cells 40 , 41 . Our study provided a new case to this field and showed that the mechanism of Sal was not limited to apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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Salinomycin induces autophagic cell death in salinomycin-sensitive melanoma cells through inhibition of autophagic flux

Liu

Hao

et al. 2020

Sci Rep

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Several literature has shown that salinomycin (Sal) is able to kill various types of cancer cells through different signaling pathways. However, its effect on melanoma has seldom been reported. We examined the anti-cancer efficacy of Sal in melanoma cell lines, and found six of eight cell lines were sensitive to Sal. Given the fact that the roles of Sal are diverse in different cancer types, we were eager to figure out the mechanism involved in the current study. We noticed the most sensitive line, SK-Mel-19, showed a typical morphological change after Sal treatment. The autophagy inhibitor, 3-MA, could effectively suppress Sal-induced cell death. It could also facilitate the increase of autophagic markers and reduce the turnover of autophagosomes, which resulted in an aberrant autophagic flux. On the other hand, Sal could stimulate endoplasmic reticulum stress and cause an accumulation of dysfunctional mitochondria. We also discovered a potential correlation between LC3B mRNA level and its sensitivity to Sal in 43 clinical melanoma samples. Overall, our results indicated that Sal could have multiple effect on melanoma cells and induce autophagic cell death in certain kinds of cells, which provided a new insight into the chemotherapy for melanoma.

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Section: Discussionmentioning

confidence: 99%

“…Membranes were incubated with primary antibody solution at 4 °C overnight after blocked, and then incubated with secondary antibody solution for an hour. Images were captured by densitometric scanning (Tanon-5500, Shanghai, China) and analyzed by ImageJ software 41 .…”

Section: Methodsmentioning

confidence: 99%

Salinomycin induces autophagic cell death in salinomycin-sensitive melanoma cells through inhibition of autophagic flux

Liu

Hao

et al. 2020

Sci Rep

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“…It seems that SI-2-based molecules are promising agents for specifically inhibiting SRC-3 in BCa, and we will probably discuss them further in the next few years. On the other hand, it was shown that salinomycin directly inhibits SRC-3 transcription and increases the sensitivity of BCa cells to tamoxifen [295]. Although salinomycin inhibits the malignant behaviors of BCa cells and kills CSCs, it isn't a specific SRC-3 inhibitor [296].…”

Section: Src-3 Is a Promising Target To Overcome Therapy Resistance I...mentioning

confidence: 99%

Critical Roles of SRC-3 in the Development and Progression of Breast Cancer, Rendering It a Prospective Clinical Target

Varisli,

Dancik,

Tolan

et al. 2023

Cancers

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Breast cancer (BCa) is the most frequently diagnosed malignant tumor in women and is also one of the leading causes of cancer-related death. Most breast tumors are hormone-dependent and estrogen signaling plays a critical role in promoting the survival and malignant behaviors of these cells. Estrogen signaling involves ligand-activated cytoplasmic estrogen receptors that translocate to the nucleus with various co-regulators, such as steroid receptor co-activator (SRC) family members, and bind to the promoters of target genes and regulate their expression. SRC-3 is a member of this family that interacts with, and enhances, the transcriptional activity of the ligand activated estrogen receptor. Although SRC-3 has important roles in normal homeostasis and developmental processes, it has been shown to be amplified and overexpressed in breast cancer and to promote malignancy. The malignancy-promoting potential of SRC-3 is diverse and involves both promoting malignant behavior of tumor cells and creating a tumor microenvironment that has an immunosuppressive phenotype. SRC-3 also inhibits the recruitment of tumor-infiltrating lymphocytes with effector function and promotes stemness. Furthermore, SRC-3 is also involved in the development of resistance to hormone therapy and immunotherapy during breast cancer treatment. The versatility of SRC-3 in promoting breast cancer malignancy in this way makes it a good target, and methodical targeting of SRC-3 probably will be important for the success of breast cancer treatment.

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“…These findings suggest that GA could be used as a potential inhibitor of SRC-3 for cancer therapy. Salinomycin, an antibiotic, was found to down-regulate the transcription of SRC-3 and increase the sensitivity of breast cancer cells to tamoxifen treatment, which indicates salinomycin may be developed as SRC-3 inhibitor for endocrine-resistant breast cancer [ 157 ]. However, it has not been examined whether GA and salinomycin have an effect on the expression of SRC-1 and SRC-2.…”

Section: Src-3 As Therapeutic Targetmentioning

confidence: 99%

SRC-3, a Steroid Receptor Coactivator: Implication in Cancer

Li¹,

Deng²,

Chen³

2021

IJMS

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Steroid receptor coactivator-3 (SRC-3), also known as amplified in breast cancer 1 (AIB1), is a member of the SRC family. SRC-3 regulates not only the transcriptional activity of nuclear receptors but also many other transcription factors. Besides the essential role of SRC-3 in physiological functions, it also acts as an oncogene to promote multiple aspects of cancer. This review updates the important progress of SRC-3 in carcinogenesis and summarizes its mode of action, which provides clues for cancer therapy.

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Salinomycin overcomes acquired tamoxifen resistance through AIB1 and inhibits cancer cell invasion in endocrine resistant breast cancer

Cited by 10 publications

References 54 publications

Salinomycin induces autophagic cell death in salinomycin-sensitive melanoma cells through inhibition of autophagic flux

Salinomycin induces autophagic cell death in salinomycin-sensitive melanoma cells through inhibition of autophagic flux

Critical Roles of SRC-3 in the Development and Progression of Breast Cancer, Rendering It a Prospective Clinical Target

SRC-3, a Steroid Receptor Coactivator: Implication in Cancer

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