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Alantolactone inhibits stem-like cell phenotype, chemoresistance and metastasis in PC3 cells through STAT3 signaling
Ghader Babaei1, Mohammad Hassan Khadem Ansari1,2, Shiva Gholizadeh-Ghaleh Aziz1
1Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, I.R. Iran.
Background And Purpose:
Cancer stem cells (CSCs), as the subpopulation of cancer cells, are associated with carcinogenesis, chemoresistance, and metastasis in malignancies. Also, CSCs are considered as the major reason for treatment failure in prostate cancer (PCa). Alantolactone (ALT), exerts anticancer activity in different types of cancers. In the present study, the relationship between ALT and CSCs in PCa metastasis and the molecular mechanisms involved in the progression of PCa were investigated.
Experimental Approach:
In this study, to evaluate cell viability, MTT assay was performed. Then, PC3 cells were treated with nontoxic concentrations of ALT and after this step wound-healing assay, colony-formation assay and chemosensitization assay were applied to determine cell migration, the ability of colony formation, and chemoresistance, respectively. Also, real-time polymerase chain reaction and western blotting were used for the determination of genes and protein expression, respectively.
Findings/Results:
Our finding showed that ALT at nontoxic concentrations (0.01 and 0.1 μM) for 72 h suppressed the STAT3 phosphorylation and signaling pathway. Also, ALT was able to modulate the stemness of PCa cells through downregulation of expression of SOX2, Oct-4, Nanog, CD133, CD44, and upregulation of p53 expression. On the other hand, we further found that ALT in nontoxic concentrations sensitized PCa cells to cisplatin.
Conclusion And Implications:
ALT combated the stemness of cancer cells and metastasis by antagonizing of STAT3 signaling pathway. In addition, ALT exhibited anti-metastatic properties and may have potential as a new chemotherapy agent for the reduction of PCa metastasis.
Insights
Alantolactone (ALT) combats prostate cancer stemness and metastasis by inhibiting the STAT3 signaling pathway. This natural compound also sensitizes cancer cells to chemotherapy, showing potential as a novel treatment agent.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Cancer stem cells (CSCs) drive malignancy, chemoresistance, and metastasis in prostate cancer (PCa).
- CSCs are a primary cause of treatment failure in PCa.
- Alantolactone (ALT) demonstrates anticancer activity across various cancer types.
Purpose of the Study:
- To investigate the effects of ALT on PCa CSCs.
- To elucidate the molecular mechanisms underlying ALT's action in PCa metastasis.
- To evaluate ALT's potential in overcoming chemoresistance and metastasis.
Main Methods:
- Cell viability assessed via MTT assay.
- Migration, colony formation, and chemoresistance evaluated using wound-healing, colony-formation, and chemosensitization assays.
- Gene and protein expression analyzed by real-time PCR and Western blotting.
Main Results:
- ALT (0.01–0.1 μM) suppressed STAT3 phosphorylation and signaling.
- ALT modulated PCa cell stemness by downregulating SOX2, Oct-4, Nanog, CD133, CD44, and upregulating p53.
- ALT sensitized PCa cells to cisplatin treatment.
Conclusions:
- ALT inhibits CSC stemness and metastasis by antagonizing the STAT3 pathway.
- ALT possesses anti-metastatic properties.
- ALT shows promise as a novel chemotherapeutic agent for reducing PCa metastasis.
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