Resveratrol as an Enhancer of Apoptosis in Cancer: A Mechanistic Review

2020 ◽  
Vol 20 ◽  
Author(s):  
Milad Ashrafizadeh ◽  
Shahram Taeb ◽  
Hamed Haghi-Aminjan ◽  
Shima Afrashi ◽  
Kave Moloudi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Fas Ligand ◽  
Inhibitory Effect ◽  
Mitochondrial Pathway ◽  
Multi Drug Resistance ◽  
Chemotherapy Drugs ◽  
Normal Tissues ◽  
Anti Cancer

: Resistance of cancer cells to therapy is a challenge for achieving an appropriate therapeutic outcome. Cancer (stem) cells possess several mechanisms for increasing their survival following exposure to toxic agents such as chemotherapy drugs, radiation as well as immunotherapy. Evidences show that apoptosis plays a key role in response of cancer (stem) cells and their multi drug resistance. Modulation of both intrinsic and extrinsic pathways of apoptosis can increase efficiency of tumor response and amplify the therapeutic effect of radiotherapy, chemotherapy, targeted therapy and also immunotherapy. To date, several agents as adjuvant have been proposed to overcome resistance of cancer cells to apoptosis. Natural products are interesting because of low toxicity on normal tissues. Resveratrol is a natural herbal agent that has shown interesting anti-cancer properties. It has been shown to kill cancer cells selectively, while protecting normal cells. Resveratrol can augment reduction/oxidation (redox) reactions, thus increases the production of ceramide and the expression of apoptosis receptors such as Fas ligand (FasL). Resveratrol also triggers some pathways which induce mitochondrial pathway of apoptosis. On the other hand, resveratrol has an inhibitory effect on anti-apoptotic mediators such as nuclear factor κ B (NFκB), cyclooxygenase-2 (COX-2), phosphatidylinositol 3–kinase (PI3K) and mTOR. In this review, we explain the modulatory effects of resveratrol on apoptosis, which can augment the therapeutic efficiency of anti-cancer drugs or radiotherapy.

scholarly journals Combinatory Effect of Jerantinine A and Chemotherapeutic Agent in Regulating Spliceosome in Breast Cancer Stem Cells and Non-Stem Breast Cancer Cells

2018 ◽  
Vol 4 (Supplement 2) ◽  
pp. 218s-218s
Author(s):  
C.H. Tan ◽  
C.W. Mai ◽  
C.O. Leong
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Drug Combination ◽  
Breast Cancer Cells ◽  
Inhibitory Effect ◽  
Chemotherapeutic Agents ◽  
Combination Effect ◽  
Breast Cancer Stem Cells

Background: Breast cancer is the second most common cancer and is afflicting women globally. Current standard regimen of chemotherapy includes 2 main classes of drug anthracycline (e.g., doxorubicin) and taxane (e.g., paclitaxel). Two main issues are associated with these drugs: toxicity and recurrence. The former issue warrants for search of novel compounds which preferably synergize with the existing chemotherapeutic agents. Whereas the latter prompts researchers to test their anticancer compounds against breast cancer stem cells (BCSCs), which is the culprit behind tumorigenesis. In a preliminary study, an indole alkaloid compound named Jerantinine A (JA) was found to have anticancer effect on breast cancer cells. The effect was mediated by disruption of splicing in the cancer cells. The key spliceosome component involved was splicing factor 3b subunit 1 (SF3b1). Aim: In current study, we further investigated whether JA had similar inhibitory effect on BCSCs. Also, if such inhibitory effect was mediated by SF3b1 too. Lastly, we explored the drug combination effect of doxorubicin and JA. Methods: Cell proliferative assay was used to determine viability of BCSCs, which would indicate the inhibitory effect of JA. On the other hand, quantitative polymerase chain reaction (qPCR) was used in detection of disrupted spliceosome activity, especially that associated with SF3b1. With respect to drug combination effect, the Chou and Talalay method was used in the relevant analysis. Results: Results showed that JA had inhibitory effect on BCSCs in vitro. Such effect was mediated by SF3b1, as shown by accumulation of 4 associated unspliced premRNAs (e.g., RIOK3, BRD2, DNAJB1, CDKN1B) in quantitative-PCR (qPCR). Lastly, based on the combined index (CI) and drug reduction index (DRI), we concluded that JA not only could synergize with doxorubicin but also sensitized BCSCs to the effect of doxorubicin. Conclusion: There was a main caveat, which was the ratio of JA against doxorubicin; only at certain ratios did the combinatory effect therefor hold promising. Nonetheless, our findings provided basis for future studies to look further into the potential of JA in alleviating cardiotoxicity issue of doxorubicin and the roles of spliceosome in breast cancer.

Targeting Nodal and Cripto-1: Perspectives Inside Dual Potential Theranostic Cancer Biomarkers

2019 ◽  
Vol 26 (11) ◽  
pp. 1994-2050 ◽  
Author(s):  
Annamaria Sandomenico ◽  
Menotti Ruvo
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Normal Development ◽  
Cancer Biomarkers ◽  
Normal Tissues ◽  
Tumor Relapse ◽  
Developmental Factors ◽  
Theranostic Agents ◽  
Tumor Types ◽  
Embryonic Signaling

Background:Elucidating the mechanisms of recurrence of embryonic signaling pathways in tumorigenesis has led to the discovery of onco-fetal players which have physiological roles during normal development but result aberrantly re-activated in tumors. In this context, Nodal and Cripto-1 are recognized as onco-developmental factors, which are absent in normal tissues but are overexpressed in several solid tumors where they can serve as theranostic agents.Objective:To collect, review and discuss the most relevant papers related to the involvement of Nodal and Cripto-1 in the development, progression, recurrence and metastasis of several tumors where they are over-expressed, with a particular attention to their occurrence on the surface of the corresponding sub-populations of cancer stem cells (CSC).Results:We have gathered, rationalized and discussed the most interesting findings extracted from some 370 papers related to the involvement of Cripto-1 and Nodal in all tumor types where they have been detected. Data demonstrate the clear connection between Nodal and Cripto-1 presence and their multiple oncogenic activities across different tumors. We have also reviewed and highlighted the potential of targeting Nodal, Cripto-1 and the complexes that they form on the surface of tumor cells, especially of CSC, as an innovative approach to detect and suppress tumors with molecules that block one or more mechanisms that they regulate.Conclusion:Overall, Nodal and Cripto-1 represent two innovative and effective biomarkers for developing potential theranostic anti-tumor agents that target normal as well as CSC subpopulations and overcome both pharmacological resistance and tumor relapse.

Targeting Cancer Stem Cells and Non-Stem Cancer Cells: The Potential of Lipid- Based Nanoparticles

2018 ◽  
Vol 23 (43) ◽  
pp. 6563-6572
Author(s):  
Ana Filipa Cruz ◽  
Nuno Andre Fonseca ◽  
Vera Moura ◽  
Sergio Simoes ◽  
Joao Nuno Moreira
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells

Comparison of the Growth Curves of Cancer Cells and Cancer Stem Cells

2014 ◽  
Vol 9 (2) ◽  
pp. 112-116 ◽  
Author(s):  
Maria Toloudi ◽  
Eleni Ioannou ◽  
Marina Chatziioannou ◽  
Panagiotis Apostolou ◽  
Christos Kiritsis ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Growth Curves

scholarly journals The microRNA-210-Stathmin1 Axis Decreases Cell Stiffness to Facilitate the Invasiveness of Colorectal Cancer Stem Cells

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1833
Author(s):  
Tsai-Tsen Liao ◽  
Wei-Chung Cheng ◽  
Chih-Yung Yang ◽  
Yin-Quan Chen ◽  
Shu-Han Su ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Motility ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Cell Stiffness ◽  
Mesenchymal Transition ◽  
Cytoskeletal Dynamics ◽  
Colorectal Cancer Stem Cells

Cell migration is critical for regional dissemination and distal metastasis of cancer cells, which remain the major causes of poor prognosis and death in patients with colorectal cancer (CRC). Although cytoskeletal dynamics and cellular deformability contribute to the migration of cancer cells and metastasis, the mechanisms governing the migratory ability of cancer stem cells (CSCs), a nongenetic source of tumor heterogeneity, are unclear. Here, we expanded colorectal CSCs (CRCSCs) as colonospheres and showed that CRCSCs exhibited higher cell motility in transwell migration assays and 3D invasion assays and greater deformability in particle tracking microrheology than did their parental CRC cells. Mechanistically, in CRCSCs, microRNA-210-3p (miR-210) targeted stathmin1 (STMN1), which is known for inducing microtubule destabilization, to decrease cell elasticity in order to facilitate cell motility without affecting the epithelial–mesenchymal transition (EMT) status. Clinically, the miR-210-STMN1 axis was activated in CRC patients with liver metastasis and correlated with a worse clinical outcome. This study elucidates a miRNA-oriented mechanism regulating the deformability of CRCSCs beyond the EMT process.

scholarly journals Hampering Stromal Cells in the Tumor Microenvironment as a Therapeutic Strategy to Destem Cancer Stem Cells

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3191
Author(s):  
Katherine Po Sin Chung ◽  
Rainbow Wing Hei Leung ◽  
Terence Kin Wah Lee
Keyword(s):  
Stem Cells ◽  
Tumor Microenvironment ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Stromal Cells ◽  
Current Knowledge ◽  
Special Focus ◽  
Intrinsic Regulation ◽  
Mechanistic Basis ◽  
Novel Therapeutic Strategies

Cancer stem cells (CSCs) within the tumor bulk play crucial roles in tumor initiation, recurrence and therapeutic resistance. In addition to intrinsic regulation, a growing body of evidence suggests that the phenotypes of CSCs are also regulated extrinsically by stromal cells in the tumor microenvironment (TME). Here, we discuss the current knowledge of the interplay between stromal cells and cancer cells with a special focus on how stromal cells drive the stemness of cancer cells and immune evasive mechanisms of CSCs. Knowledge gained from the interaction between CSCs and stromal cells will provide a mechanistic basis for the development of novel therapeutic strategies for the treatment of cancers.

Codelivery of salinomycin and doxorubicin using nanoliposomes for targeting both liver cancer cells and cancer stem cells

Nanomedicine ◽  
2016 ◽  
Vol 11 (19) ◽  
pp. 2565-2579 ◽  
Author(s):  
Zhirong Gong ◽  
Dazhong Chen ◽  
Fangyuan Xie ◽  
Junjie Liu ◽  
He Zhang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Liver Cancer Cells
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