Targeting Cancer Stem Cells by Dietary Agents: An Important Therapeutic Strategy against Human Malignancies

Paskeh, Mahshid Deldar Abad; Asadi, Shafagh; Zabolian, Amirhossein; Saleki, Hossein; Khoshbakht, Mohammad Amin; Sabet, Sina; Naghdi, Mohamad Javad; Hashemi, Mehrdad; Hushmandi, Kiavash; Ashrafizadeh, Milad; Mirzaei, Sepideh; Zarrabi, Ali; Sethi, Gautam

doi:10.3390/ijms222111669

Cited by 25 publications

(18 citation statements)

References 409 publications

(412 reference statements)

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“…The testosterone-induced proliferation of human glioblastoma cells can partially elucidate the enhanced capability for colony formation. Using dietary agents, including flavonoids, pomegranate, carotenoids, sulforaphane, curcumin, resveratrol, berberine, and ginseng, to reduce the capacity of cancer stem cells and cancer cells to form colonies can simultaneously impair cancer stemness, induce apoptosis of cancer cells, and enhance sensitivity of tumors to chemotherapy and radiotherapy in vitro and in vivo [ 34 ]. Thus, testosterone AR–PARD3B signaling events may be involved in tumorigenesis and malignance of human GBM through regulating cell proliferation and colony formation.…”

Section: Discussionmentioning

confidence: 99%

Contribution of the Testosterone Androgen Receptor–PARD3B Signaling Axis to Tumorigenesis and Malignance of Glioblastoma Multiforme through Stimulating Cell Proliferation and Colony Formation

Yang

Chen

Liu

et al. 2022

JCM

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Background: Glioblastoma multiforme (GBM) is the most common and malignant brain tumor with very poor prognoses. After surgical resection of the primary tumor, rapid proliferation of residual glioblastoma cells is a critical cause explaining tumor malignance and recurrence. In this study, we evaluated de novo roles of the testosterone androgen receptor (AR)–PARD3B signaling axis in the tumorigenesis and malignance of human GBM and the possible related mechanisms. Methods: AR and PARD3B gene expressions and their correlations were mined from The Cancer Genome Atlas (TCGA) database and analyzed using the UALCAN system. Analyses using a real-time PCR, cell proliferation, and colony formation and a loss-of-function strategy by suppressing AR activity with its specific inhibitor, enzalutamide, were then carried out to determine roles of the testosterone AR–PARD3B signaling axis in tumor malignance. Results: Expressions of AR, PARD3B mRNA, and proteins in human GBM tissues were upregulated compared to normal human brain tissues. In contrast, levels of AR and PARD3B mRNA in most TCGA pan-cancer types were downregulated compared to their respective normal tissues. Interestingly, a highly positive correlation between AR and PARD3B gene expressions in human GBM was identified. The results of a bioinformatics search further showed that there were five AR-specific DNA-binding elements predicted in the 5′ promoter of the PARD3B gene. Regarding the mechanisms, exposure of human glioblastoma cells to testosterone induced AR and PARD3B gene expressions and successively stimulated cell proliferation and colony formation. Suppressing AR activity concurrently resulted in significant attenuations of testosterone-induced PARD3B gene expression, cell proliferation, and colony formation in human glioblastoma cells. Conclusions: This study showed the contribution of the testosterone AR–PARD3B signaling axis to the tumorigenesis and malignance of human GBM through stimulating cell proliferation and colony formation. Therefore, the AR-PARD3B signaling axis could be targeted for potential therapy for human GBM.

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Section: Discussionmentioning

confidence: 99%

Contribution of the Testosterone Androgen Receptor–PARD3B Signaling Axis to Tumorigenesis and Malignance of Glioblastoma Multiforme through Stimulating Cell Proliferation and Colony Formation

Yang

Chen

Liu

et al. 2022

JCM

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“…Halim et al, 2019;Kashyap et al, 2021;Li, Shanmugam et al, 2015). Furthermore, phytochemicals are affordable and developing countries can utilize them in the treatment of cancer patients (Amini et al, 2021;Ashrafizadeh, Rafiei et al, 2021;Ashrafizadeh, Zarrabi, Orouei, Saberifar et al, 2021;Deldar Abad Paskeh, Asadi et al, 2021;Hashemi et al, 2021;Hussain et al, 2021;Samec et al, 2021). This section focuses on recent studies using antitumor agents in modulating NF-κB/EMT axis.…”

Section: Ncrnas In Nf-κ B/emt Regulationmentioning

confidence: 99%

“…There are some reasons for selecting plant derived‐natural products that can be their low side effects, high safety profile, multitargeting capacity, and lack of drug resistance in tumor cells (Ahn, Sethi, & Aggarwal, 2008; F. Halim et al, 2019; Kashyap et al, 2021; Li, Shanmugam et al, 2015). Furthermore, phytochemicals are affordable and developing countries can utilize them in the treatment of cancer patients (Amini et al, 2021; Ashrafizadeh, Rafiei et al, 2021; Ashrafizadeh, Zarrabi, Orouei, Saberifar et al, 2021; Deldar Abad Paskeh, Asadi et al, 2021; Hashemi et al, 2021; Hussain et al, 2021; Samec et al, 2021). This section focuses on recent studies using antitumor agents in modulating NF‐κB/EMT axis.…”

Section: Selected Antitumor Compounds Targeting Nf‐κb/emt Axismentioning

confidence: 99%

NF‐κB as a regulator of cancer metastasis and therapy response: A focus on epithelial–mesenchymal transition

Mirzaei

Saghari

Bassiri

et al. 2022

Journal Cellular Physiology

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Metastasis of tumor cells is a complex challenge and significantly diminishes the overall survival and prognosis of cancer patients. The epithelial‐to‐mesenchymal transition (EMT) is a well‐known mechanism responsible for the invasiveness of tumor cells. A number of molecular pathways can regulate the EMT mechanism in cancer cells and nuclear factor‐kappaB (NF‐κB) is one of them. The nuclear translocation of NF‐κB p65 can induce the transcription of several genes involved in EMT induction. The present review describes NF‐κB and EMT interaction in cancer cells and their association in cancer progression. Due to the oncogenic role NF‐κB signaling, its activation enhances metastasis of tumor cells via EMT induction. This has been confirmed in various cancers including brain, breast, lung and gastric cancers, among others. The ZEB1/2, transforming growth factor‐β, and Slug as inducers of EMT undergo upregulation by NF‐κB to promote metastasis of tumor cells. After EMT induction driven by NF‐κB, a significant decrease occurs in E‐cadherin levels, while N‐cadherin and vimentin levels undergo an increase. The noncoding RNAs can potentially also function as upstream mediators and modulate NF‐κB/EMT axis in cancers. Moreover, NF‐κB/EMT axis is involved in mediating drug resistance in tumor cells. Thus, suppressing NF‐κB/EMT axis can also promote the sensitivity of cancer cells to chemotherapeutic agents.

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“…A study reported that genistein inhibits tumor growth and cell proliferation by downregulating the negative effect of epidermal growth factor (EGF) on the activity of forkhead box O3 (FOXO3) in a colon cancer model [ 79 ]. In addition, it is also observed that genistein reduces breast cancer stem cells (CSCs) and mammospheres by downregulating the hedgehog-signaling pathway that subsequently regulates cell proliferation, self-renewal ability, stem cell, and progenitor cell maintenance [ 80 , 81 ]. Based on the scientific studies, it is believed that genistein regulates miRNAs expression to stop cell proliferation and up-regulates miR-200 expression, also regulate the essential targets such as vimentin, zinc finger E-box binding homeobox 1 (ZEB1), and slug, which help in the epithelial-mesenchymal transition (EMT) process [ 82 , 83 ].…”

Section: Natural Productsmentioning

confidence: 99%

The Role of Natural Products and Their Multitargeted Approach to Treat Solid Cancer

Muhammad

Usmani²,

Tarique

et al. 2022

Cells

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Natural products play a critical role in the discovery and development of numerous drugs for the treatment of various types of cancer. These phytochemicals have demonstrated anti-carcinogenic properties by interfering with the initiation, development, and progression of cancer through altering various mechanisms such as cellular proliferation, differentiation, apoptosis, angiogenesis, and metastasis. Treating multifactorial diseases, such as cancer with agents targeting a single target, might lead to limited success and, in many cases, unsatisfactory outcomes. Various epidemiological studies have shown that the steady consumption of fruits and vegetables is intensely associated with a reduced risk of cancer. Since ancient period, plants, herbs, and other natural products have been used as healing agents. Likewise, most of the medicinal ingredients accessible today are originated from the natural resources. Regardless of achievements, developing bioactive compounds and drugs from natural products has remained challenging, in part because of the problem associated with large-scale sequestration and mechanistic understanding. With significant progress in the landscape of cancer therapy and the rising use of cutting-edge technologies, we may have come to a crossroads to review approaches to identify the potential natural products and investigate their therapeutic efficacy. In the present review, we summarize the recent developments in natural products-based cancer research and its application in generating novel systemic strategies with a focus on underlying molecular mechanisms in solid cancer.

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Targeting Cancer Stem Cells by Dietary Agents: An Important Therapeutic Strategy against Human Malignancies

Cited by 25 publications

References 409 publications

Contribution of the Testosterone Androgen Receptor–PARD3B Signaling Axis to Tumorigenesis and Malignance of Glioblastoma Multiforme through Stimulating Cell Proliferation and Colony Formation

Contribution of the Testosterone Androgen Receptor–PARD3B Signaling Axis to Tumorigenesis and Malignance of Glioblastoma Multiforme through Stimulating Cell Proliferation and Colony Formation

NF‐κB as a regulator of cancer metastasis and therapy response: A focus on epithelial–mesenchymal transition

The Role of Natural Products and Their Multitargeted Approach to Treat Solid Cancer

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