The natural flavonoid silybin improves the response to Photodynamic Therapy of bladder cancer cells

Gándara, Lautaro; Sandes, Eduardo Omar; Venosa, Gabriela Di; McCormick, Barbara Prack; Rodríguez, Lorena; Mamone, Leandro; Batlle, Alcira; Eiján, Ana María; Casas, Adriana

doi:10.1016/j.jphotobiol.2014.03.006

Cited by 40 publications

(24 citation statements)

References 57 publications

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“…According to the American Cancer Society, the primary therapies for bladder carcinoma include surgery, intravesicular therapy, chemotherapy, and radiation therapy [203]. Newer treatments include photodynamic therapy, gene therapy, and targeted drug therapies [79,203]. …”

Section: Immunological Basis Of the Treatment Strategies In Bladder Cmentioning

confidence: 99%

Immunological basis in the pathogenesis and treatment of bladder cancer

Thompson

Siref

Feloney

et al. 2014

Expert Review of Clinical Immunology

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The pathogenesis and transition of normal urothelium into bladder carcinoma are multifactorial processes. Chronic inflammation causes initiation and progression of the underlying pathophysiology of invasive and metastatic cancer. A dichotomy is observed in the role of immune cells in bladder cancer. While the immune response defends the host by suppressing neoplastic growth, several immune cells, including neutrophils, macrophages, and T-lymphocytes, promote tumor development and progression. The levels of human neutrophil peptide-1, -2, and -3, produced by neutrophils, increase in bladder cancer and might promote tumor angiogenesis and growth. The effect of macrophages is primarily mediated by pro-inflammatory cytokines, IL-6 and TNF-α. Additionally, the underlying immunological mechanisms of two treatments, BCG and cytokine gene-modified tumor vaccines, and future directions are critically discussed.

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Section: Immunological Basis Of the Treatment Strategies In Bladder Cmentioning

confidence: 99%

Immunological basis in the pathogenesis and treatment of bladder cancer

Thompson

Siref

Feloney

et al. 2014

Expert Review of Clinical Immunology

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“…1) is a biologically active component extracted from the seeds of milk thistle, Silybum marianum, and its derivatives have been demonstrated to exhibit marked anti-cancer activity (6). In-vitro studies have shown that silybin inhibits androgen-dependent and -independent prostate cancer as well as skin, bladder, lung, colon, breast, ovarian, renal, liver, cervical and tongue cancer (7)(8)(9). However, the anti-cancer effects of silybin on MM cells and its underlying mechanisms of action have not yet been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Silybin suppresses cell proliferation and induces apoptosis of multiple myeloma cells via the PI3K/Akt/mTOR signaling pathway

Feng

Luo

Guo

2016

Molecular Medicine Reports

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Abstract. Silybin is a biologically active component extracted from the seeds of Silybum marianum, which has been shown to have inhibitory effects on prostate, skin, bladder, lung and colon cancer cells, in addition to its efficacy in the treatment of liver diseases, including hepatitis and cirrhosis. The aim of the present study was to investigate whether silybin suppresses the proliferation and induces apoptosis of multiple myeloma (MM) cells and to elucidate its molecular targets. The proliferative and apoptotic rates of the U266 MM cell line were assessed using MTT and flow-cytometric assays, respectively. Western blot analysis was used to assess the protein levels of phosphoinositide-3 kinase (PI3K), phosphorylated (p)-Akt and p-mammalian target of rapamycin (mTOR) in U266 cells. In addition, PI3K inhibitor LY294002 or activator insulin-like growth factor 1 were used to investigate the involvement of the PI3K/Akt-mTOR signaling pathway in the effect of silybin on U266 cells. The results revealed that silybin restrained the proliferation and enhanced the apoptosis of U266 cells. Furthermore, silybin inhibited the protein expression of PI3K, p-Akt and p-mTOR in U266 cells. Of note, inhibition of PI3K facilitated silybin-mediated reduction of mTOR activation, cell proliferation and induction of apoptosis in U266 cells, while activation of PI3K attenuated the effects of silybin. In conclusion, silybin suppressed cell proliferation and promoted apoptosis of U266 cells via PI3K/Akt-mTOR signaling pathways.

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“…1A), a natural polyphenolic flavonoid, is a major bioactive component of silymarin isolated from the plant milk thistle Silybum marianum (L.) Gaertn. Silibinin has been extensively used for its hepatoprotective effectiveness in Asia and Europe (3,4). According to the reports, flavonoids have been shown to be cytotoxic to cancer cells (5,6).…”

Section: Introductionmentioning

confidence: 99%

ERα down-regulation plays a key role in silibinin-induced autophagy and apoptosis in human breast cancer MCF-7 cells

Zheng

Zhang

Huang

et al. 2015

Journal of Pharmacological Sciences

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The estrogen receptor alpha (ERα) has been proven to be one of the most important therapeutic targets in breast cancer over the last 30 years. Previous studies pointed out that a natural flavonoid, silibinin, induced apoptosis in human breast cancer MCF-7 cells. In the present study we report that exposure of MCF-7 cells to silibinin led to cell death through the down-regulation of ERα expression. Silibinin-induced apoptosis of MCF-7 cells through up-regulation of caspase 6 due to ERα signalling repression was further boosted by ERα antagonist. Moreover, up-regulation of autophagy induced by silibinin accounted for apoptotic exacerbation, being further enhanced by ERα inhibition. Upon ERα activation, series of downstream signalling pathways can be activated. We found that silibinin reduced the expressions of Akt/mTOR and extracellular-signal-related kinase (ERK), which respectively accounted for the induction of autophagy and apoptosis. These effects were further augmented by co-treatment with ERα inhibitor. We conclude that the treatment with silibinin of ERα-positive MCF-7 cells down-regulates the expression of ERα, and subsequently mTOR and ERK signaling pathways, ERα downstream, finally resulting in induction of autophagy and apoptosis.

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The natural flavonoid silybin improves the response to Photodynamic Therapy of bladder cancer cells

Cited by 40 publications

References 57 publications

Immunological basis in the pathogenesis and treatment of bladder cancer

Immunological basis in the pathogenesis and treatment of bladder cancer

Silybin suppresses cell proliferation and induces apoptosis of multiple myeloma cells via the PI3K/Akt/mTOR signaling pathway

ERα down-regulation plays a key role in silibinin-induced autophagy and apoptosis in human breast cancer MCF-7 cells

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