Silibinin exerts anti-cancer activity on human ovarian cancer cells by increasing apoptosis and inhibiting epithelial-mesenchymal transition (EMT)

Maleki, Narges; Yavari, Negar; Ebrahimi, Maryam; Faiz, Ahmad Faisal; Ravesh, Roya Khosh; Sharbati, Aysan; Panji, Mohammad; Lorian, Keivan; Gravand, Abdollah; Abbasi, Mojtaba; Abazari, Omid; Mehr, Mehdi Shafiee; Eskandari, Yasin

doi:10.1016/j.gene.2022.146275

Cited by 16 publications

(6 citation statements)

References 55 publications

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“…Recently, Si et al disclosed that silibinin treatment promoted mitochondrial fusion by suppressing the expression of DRP1 and enhancing the expression of Mfn1, Mfn2, and OPA1, leading to attenuated migration and invasion of breast cancer cells [ 94 ]. Additionally, silibinin plays an important role in other cancer cells such as colorectal cancer [ 95 ], ovarian cancer [ 96 ], and lung cancer [ 97 ] cells, and could serve as a potential therapeutic biomolecule. Doxorubicin (Dox) is a highly effective chemotherapy drug used to treat solid tumors and hematological malignancies.…”

Section: Resultsmentioning

confidence: 99%

Roles of mitochondrial fusion and fission in breast cancer progression: a systematic review

Xing

Liu

et al. 2022

World J Surg Onc

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Background Mitochondria play critical roles in cellular physiological activity as cellular organelles. Under extracellular stimulation, mitochondria undergo constant fusion and fission to meet different cellular demands. Mitochondrial dynamics, which are involved in mitochondrial fusion and fission, are regulated by specialized proteins and lipids, and their dysregulation causes human diseases, such as cancer. The advanced literature about the crucial role of mitochondrial dynamics in breast cancer is performed. Methods All related studies were systematically searched through online databases (PubMed, Web of Science, and EMBASE) using keywords (e.g., breast cancer, mitochondrial, fission, and fusion), and these studies were then screened through the preset inclusion and exclusion criteria. Results Eligible studies (n = 19) were evaluated and discussed in the systematic review. These advanced studies established the roles of mitochondrial fission and fusion of breast cancer in the metabolism, proliferation, survival, and metastasis. Importantly, the manipulating of mitochondrial dynamic is significant for the progresses of breast cancer. Conclusion Understanding the mechanisms underlying mitochondrial fission and fusion during tumorigenesis is important for improving breast cancer treatments.

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Section: Resultsmentioning

confidence: 99%

Roles of mitochondrial fusion and fission in breast cancer progression: a systematic review

Xing

Liu

et al. 2022

World J Surg Onc

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“…García-Cabo et al also demonstrated that the expression level of β-Catenin is a risk factor for poor prognosis in laryngeal cell carcinoma [34]. Moreover, the inactivation of the Wnt/ β-Catenin pathway promotes apoptotic cell death in human ovarian cancer cells [35]. In addition, chemical drugs inhibiting Wnt/β-Catenin pathway or small interfering RNA targeting β-Catenin expression could induce apoptosis [36].…”

Section: Discussionmentioning

confidence: 98%

Caudatin Inhibits the Proliferation, Invasion, and Glycolysis of Osteosarcoma Cells via the Wnt/β- Catenin Pathway

Zhang

Sheng

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Background. Caudatin is a steroidal glycoside with reported anticancer activity in a variety of studies. Nevertheless, the role and mechanisms of caudatin in osteosarcoma (OS) remain unclear. In this study, we explored the potential anticancer effects of caudatin in OS cells and investigated the underlying mechanisms. Methods. Both the CCK8 proliferation assay and flow cytometry were employed to evaluate cell proliferation and apoptosis. A transwell assay was applied to determine cell invasion ability. Besides, glycolytic capacity was examined by measuring glucose consumption, lactic acid production, as well as ATP production. A western blot was utilized to assess the protein levels of β-catenin, CyclinD 1, C-myc, HK2 (Hexokinase 2), LDHA (lactate dehydrogenase), as well as epithelial-mesenchymal transition (EMT)-related markers. The inhibitory effect of caudatin on tumor growth was investigated using a xenograft tumorigenesis model. Results. Caudatin restrained cellular glycolysis, suppressed cell proliferation and invasion by reducing HK2 and LDHA expression and regulating the Wnt/β-Catenin signaling pathway. Caudatin treatment caused the upregulation of E-cadherin and suppressed N-cadherin expression. Further, caudatin treatment impaired cell viability, invasion ability, and intracellular glycolysis level but induced apoptosis. The administration of BML 284 reversed the inhibitory effects of caudatin. Moreover, caudatin suppressed the tumorigenesis of OS cells in the xenograft model of nude mice. Conclusions. Our study revealed the anticancer effects of caudatin, including proliferation inhibition, cell invasion suppression, and glycolysis impairment. These effects seem to be executed through targeting the Wnt/β-Catenin signaling pathway. These data indicate that caudatin may be formulated as a potential therapeutic for osteosarcoma.

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“…Silibinin is well-tolerated by the body and has proven less toxic than other anticancer therapeutics (7). Maleki et al showed that silibinin inhibited cell growth and promoted apoptosis and reversion of the epithelial-mesenchymal transition in SKOV-3 and A2870 ovarian cancer cell lines (14). Another study reported that silibinin induced G2/M cell cycle arrest in Hela and SiHa cervical cancer cell lines via activation of the mitochondrial fission pathway (15).…”

Section: Introductionmentioning

confidence: 99%

Silibinin Induces Apoptosis and G2/M Cell Cycle Arrest in Human Ovarian Cancer SKOV-3 Cell Line

Baghal Sadriforoush,

Jahanafrooz,

Motamed

2023

Jentashapir J Cell Mol Biol

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Background: Silibinin, an herbal polyphenolic flavonolignan, has antioxidant and anticancer properties. Objectives: This study aimed to evaluate some cellular and molecular effects of silibinin on the human ovarian cancer SKOV-3 cell line. Methods: For cytotoxicity investigations of silibinin, MTT assay was used at 24, 48, and 72 hours. Apoptosis and cell cycle were studied by flow cytometry. The effect of silibinin on mRNA expression of B-cell lymphoma 2 (Bcl-2), cyclin E, and S-phase kinase-associated protein 2 (SKP2) was determined by Quantitative reverse transcription polymerase chain reaction (QRT-PCR). Results: Silibinin administration in lower concentrations (12.5 and 25 µg/mL) did not lead to significant (P < 0.05) changes in cell viability and even slightly increased cell growth after 72 hours. However, silibinin in higher concentrations (≥ 50µg/mL) inhibited SKOV-3 cell proliferation in a dose- and time-dependent manner. The mode of cell growth inhibition was apoptosis induction and G2/M cell cycle arrest. Silibinin caused down-regulation of the anti-apoptotic gene, namely Bcl-2. Additionally, silibinin resulted in down-regulation of the major genes in the cell cycle, including cyclin E and SKP2. Conclusions: Overall, this study confirmed the ability of silibinin to suppress ovarian cancer progression through the induction of apoptosis and inhibition of G2/M phase transition. Silibinin may be considered an efficient and safe herbal medication for ovarian cancer.

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Silibinin exerts anti-cancer activity on human ovarian cancer cells by increasing apoptosis and inhibiting epithelial-mesenchymal transition (EMT)

Cited by 16 publications

References 55 publications

Roles of mitochondrial fusion and fission in breast cancer progression: a systematic review

Roles of mitochondrial fusion and fission in breast cancer progression: a systematic review

Caudatin Inhibits the Proliferation, Invasion, and Glycolysis of Osteosarcoma Cells via the Wnt/β- Catenin Pathway

Silibinin Induces Apoptosis and G2/M Cell Cycle Arrest in Human Ovarian Cancer SKOV-3 Cell Line

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