scholarly journals The Role of Curcumin in Cancer Treatment

Biomedicines ◽  
2021 ◽  
Vol 9 (9) ◽  
pp. 1086
Author(s):  
Vasiliki Zoi ◽  
Vasiliki Galani ◽  
Georgios D. Lianos ◽  
Spyridon Voulgaris ◽  
Athanasios P. Kyritsis ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Molecular Mechanisms ◽  
Curcuma Longa ◽  
Immune Modulators ◽  
Anticancer Properties ◽  
Stat3 Signaling ◽  
Anticancer Effects ◽  
Transcription 3 ◽  
Light Chain Enhancer

Curcumin is a polyphenol extracted from the rhizomes of the turmeric plant, Curcuma longa which has anti-inflammatory, and anticancer properties. Chronic inflammation is associated with the development of cancer. Curcumin acts on the regulation of various immune modulators, including cytokines, cyclooxygenase-2 (COX-2), and reactive oxygen species (ROS), which partly explains its anticancer effects. It also takes part in the downregulation of growth factors, protein kinases, oncogenic molecules and various signaling pathways, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), c-Jun N-terminal kinase (JNK) and signal transducer and activator of transcription 3 (STAT3) signaling. Clinical trials of curcumin have been completed or are ongoing for various types of cancer. This review presents the molecular mechanisms of curcumin in different types of cancer and the evidence from the most recent clinical trials.

scholarly journals The p53/miR-34a/SIRT1 Positive Feedback Loop in Quercetin-Induced Apoptosis

2015 ◽  
Vol 35 (6) ◽  
pp. 2192-2202 ◽  
Author(s):  
Guohua Lou ◽  
Yanning Liu ◽  
Shanshan Wu ◽  
Jihua Xue ◽  
Fan Yang ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Feedback Loop ◽  
Molecular Mechanisms ◽  
Rt Pcr ◽  
Cycle Arrest ◽  
Anticancer Effects ◽  
Huh7 Cells ◽  
Mirnas Expression ◽  
Induced Apoptosis

Background: The anti-tumor effects of quercetin have been reported, but the underlying molecular mechanisms remain to be elucidated. The aim of present study was to explore the role of miRNA in the anticancer effects of quercetin. Methods: The differential miRNAs expression between the HepG2 and Huh7 cells treated by quercetin were detected by microarray. The xCELLigence, Flow cytometry, RT-PCR and Western blot were used to analyze the cell proliferation, cell apoptosis, cell cycle arrest, anti-tumor genes, and protein expression. Results: miR-34a was up-regulated in HepG2 cells treated by quercetin exhibiting wild-type p53. When inhibiting the miR-34a, the sensitivity of the cells to quercetin decreased and the expression of the SIRT1 was up-regulated, but the acetylation of p53 and the expression of some genes related to p53 down-regulated. Conclusion: miR-34a plays an important role in the anti-tumor effects of querctin in HCC, miR-34a may be a tiemolecule between the p53 and SIRT1 and is composed of a p53/miR-34a/SIRT1 signal feedback loop, which could enhance apoptosis signal and significantly promote cell apoptosis.

scholarly journals PhyllanthusSuppresses Prostate Cancer Cell, PC-3, Proliferation and Induces Apoptosis through Multiple Signalling Pathways (MAPKs, PI3K/Akt, NFκB, and Hypoxia)

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Yin-Quan Tang ◽  
InduBala Jaganath ◽  
Rishya Manikam ◽  
Shamala Devi Sekaran
Keyword(s):  
Molecular Mechanisms ◽  
Prostate Cancer Cell ◽  
Prostate Adenocarcinoma ◽  
Signalling Pathways ◽  
Differentially Expressed Proteins ◽  
Signalling Molecules ◽  
Anticancer Properties ◽  
Anticancer Effects ◽  
2D Gel

Phyllanthusis a traditional medicinal plant that has been found to have antihepatitis, antibacterial, and anticancer properties. The present studies were to investigate thein vitromolecular mechanisms of anticancer effects ofPhyllanthus(P. amarus, P. niruri, P. urinaria,andP. watsonii) plant extracts in human prostate adenocarcinoma. The cancer ten-pathway reporter array was performed and revealed that the expression of six pathway reporters were significantly decreased (Wnt, NFκB, Myc/Max, hypoxia, MAPK/ERK, and MAPK/JNK) in PC-3 cells after treatment withPhyllanthusextracts. Western blot was conducted and identified several signalling molecules that were affected in the signalling pathways including pan-Ras, c-Raf, RSK, Elk1, c-Jun, JNK1/2, p38 MAPK, c-myc, DSH,β-catenin, Akt, HIF-1α, GSK3β, NFκB p50 and p52, Bcl-2, Bax, and VEGF, in treated PC-3 cells. A proteomics-based approach, 2D gel electrophoresis, was performed, and mass spectrometry (MS/MS) results revealed that there were 72 differentially expressed proteins identified in treated PC-3 cells and were involved in tumour cell adhesion, apoptosis, glycogenesis and glycolysis, metastasis, angiogenesis, and protein synthesis and energy metabolism. Overall, these findings suggest thatPhyllanthuscan interfere with multiple signalling cascades involved in tumorigenesis and be used as a potential therapeutic candidate for treatment of cancer.

scholarly journals miR-196b-5p-mediated downregulation of FAS promotes NSCLC progression by activating IL6-STAT3 signaling

2020 ◽  
Vol 11 (9) ◽  
Author(s):  
Xiangjie Huang ◽  
Sisi Xiao ◽  
Xinping Zhu ◽  
Yun Yu ◽  
Meng Cao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Lung Cancer Cell ◽  
Nsclc Tissue ◽  
Cancer Cell Growth ◽  
Tissue Samples ◽  
Stat3 Signaling ◽  
Transcription 3

Abstract Our recent study demonstrated that the QKI-5 regulated miRNA, miR-196b-5p, and it functions as an onco-microRNA in non-small cell lung cancer (NSCLC) by directly targeting GATA6 and TSPAN12. However, the role of miR-196b-5p in NSCLC progression and metastasis still remains unclear. We found that miR-196b-5p promotes lung cancer cell proliferation and colony formation by directly targeting tumor suppressor, FAS. The expression of FAS was significantly downregulated in NSCLC tissue samples and was negatively correlated with the miR-196b-5p expression. Knocking down FAS activates NFkB signaling and subsequent IL6 secretion, resulting in phosphorylation of signal transducer and activator of transcription 3 (STAT3) to promote lung cancer cell growth. Our findings indicated that miR-196b-5p might exhibit novel oncogenic function by FAS-mediated STAT3 activation in NSCLC, and suggested that targeting the miR-196b-5p/FAS/NFkB/IL6/STAT3 pathway might be a promising therapeutic strategy in treating NSCLC.

scholarly journals MiR-145-5p Inhibits the Invasion of Prostate Cancer and Induces Apoptosis by Inhibiting WIP1

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Jianming Sun ◽  
Linggang Deng ◽  
Ye Gong
Keyword(s):  
Prostate Cancer ◽  
Molecular Mechanisms ◽  
Quantitative Polymerase Chain Reaction ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Luciferase Reporter Gene ◽  
Anticancer Effects ◽  
Polymerase Chain

Prostate cancer (PCa) is a common malignant tumor of the male genitourinary system that seriously affects the quality of life of patients. Studying the pathogenesis and therapeutic targets of PCa is important. In this study, we investigated the role of miR-145-5p in PCa and its potential molecular mechanisms. The expression levels of miR-145-5p in PCa tissues and adjacent control tissues were detected by real-time quantitative polymerase chain reaction. The effects of miR-145-5p overexpression on PCa were studied using cell proliferation, migration, and invasion experiments. Furthermore, WIP1 was the target gene of miR-145-5p through the bioinformatics website and dual-luciferase reporter gene experiment. Further studies found that WIP1 downregulation could inhibit the proliferation, invasion, and cloning of PCa cells. Overexpression of WIP1 reversed the anticancer effects of miR-145. The anticancer effect of miR-145 was achieved by inhibiting the PI3K/AKT signaling pathway and upregulating ChK2 and p-p38MAPK. Taken together, these results confirmed that miR-145-5p inhibited the growth and metastasis of PCa cells by inhibiting the expression of proto-oncogene WIP1, thereby playing a role in tumor suppression in PCa and may become a potential therapeutic target for the treatment of PCa.

scholarly journals L1CAM promotes ovarian cancer stemness and tumor initiation via FGFR1/SRC/STAT3 signaling

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Marco Giordano ◽  
Alessandra Decio ◽  
Chiara Battistini ◽  
Micol Baronio ◽  
Fabrizio Bianchi ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Genetic Manipulation ◽  
Tumor Formation ◽  
In Vitro Assays ◽  
Tumor Initiation ◽  
Loss Of Function ◽  
Stat3 Signaling

Abstract Background Cancer stem cells (CSC) have been implicated in tumor progression. In ovarian carcinoma (OC), CSC drive tumor formation, dissemination and recurrence, as well as drug resistance, thus contributing to the high death-to-incidence ratio of this disease. However, the molecular basis of such a pathogenic role of ovarian CSC (OCSC) has been elucidated only to a limited extent. In this context, the functional contribution of the L1 cell adhesion molecule (L1CAM) to OC stemness remains elusive. Methods The expression of L1CAM was investigated in patient-derived OCSC. The genetic manipulation of L1CAM in OC cells provided gain and loss-of-function models that were then employed in cell biological assays as well as in vivo tumorigenesis experiments to assess the role of L1CAM in OC cell stemness and in OCSC-driven tumor initiation. We applied antibody-mediated neutralization to investigate L1CAM druggability. Biochemical approaches were then combined with functional in vitro assays to study the molecular mechanisms underlying the functional role of L1CAM in OCSC. Results We report that L1CAM is upregulated in patient-derived OCSC. Functional studies showed that L1CAM promotes several stemness-related properties in OC cells, including sphere formation, tumor initiation and chemoresistance. These activities were repressed by an L1CAM-neutralizing antibody, pointing to L1CAM as a druggable target. Mechanistically, L1CAM interacted with and activated fibroblast growth factor receptor-1 (FGFR1), which in turn induced the SRC-mediated activation of STAT3. The inhibition of STAT3 prevented L1CAM-dependent OC stemness and tumor initiation. Conclusions Our study implicate L1CAM in the tumorigenic function of OCSC and point to the L1CAM/FGFR1/SRC/STAT3 signaling pathway as a novel driver of OC stemness. We also provide evidence that targeting this pathway can contribute to OC eradication.

Crocetin as an Active Secondary Metabolite of Saffron Stigma and Anticancer Effects

2019 ◽  
Vol 15 (3) ◽  
pp. 192-196
Author(s):  
Ali Farahi ◽  
Homa Mollaei ◽  
Reyhane Hoshyar
Keyword(s):  
Adjuvant Therapy ◽  
Molecular Mechanisms ◽  
Synergistic Effects ◽  
Model Organisms ◽  
Epigenetic Changes ◽  
Anticancer Properties ◽  
Anticancer Effects ◽  
Therapeutic Procedures ◽  
Apoptotic Effects ◽  
Chemotherapy Agents

In order to try to increase the effectiveness of cancer therapeutic procedures, natural carotenoids attract lots of attention. Crocetin is one of the main carotenoids of saffron whose anticancer properties have been shown in recent decades. This study aimed to review previous invitro and invivo investigations on anticancer effects of this carotenoid and also proposed molecular mechanisms of its action. Literature reviewing between 1990 and 2017 was performed using pubmed and scopus databases. Anti-proliferative and pro-apoptotic effects of crocetin have been observed in several cancers cell lines and also model organisms that might be due to the alternation in the expression of cancer-related genes and epigenetic changes. Moreover, several studies indicated synergistic effects of crocetin with common chemotherapy agents and mentioned it as a potential novel adjuvant therapy.

Repurposing of Metformin for Cancer Therapy: Updated Patent and Literature Review

2021 ◽  
Vol 16 ◽  
Author(s):  
Zainab Sabry Othman Ahmed ◽  
Matthew Golovoy ◽  
Yassen Abdullah ◽  
Reda Saber Ibrahim Ahmed ◽  
Q. Ping Dou
Keyword(s):  
Clinical Trials ◽  
Cancer Therapy ◽  
Late Phase ◽  
Drug Dosage ◽  
Great Promise ◽  
Cancer Therapies ◽  
Anticancer Properties ◽  
Anticancer Effects ◽  
Pubmed Database ◽  
Early Phase Clinical Trials

Background: Over recent years, there has been an increasing focus on the repurposing of existing, well-known medications for new, novel usage. One such drug is metformin, typically utilized in the management of diabetes, which demonstrates a positive relationship between its administration and lower cancer morbidity and mortality. Based on this finding, numerous studies and clinical trials have been conducted to examine the potential usage of metformin as an anticancer agent. Objective: This article aims to summarize metformin’s anticancer effects through reviewing its literature and patents, with a focus on its potential to be repurposed for cancer therapy. Methods: Various databases were examined using keywords, ‘Metformin’ and ‘Cancer’. Research articles were collected through the PubMed database, clinical trials were obtained from the Clinical Trials database, and patents were collected through the Google Patents database. Results: Metformin shows antineoplastic activity in various models. These anticancer properties appear to synergize with existing chemotherapeutics, which allows for a reduction in drug dosage without losing potency while minimizing adverse effects. Numerous patents on metformin have been filed which claim various combination therapies, delivery methods, and uses for cancer therapy, displaying an increasing interest in metformin’s anticancer potential. Conclusion: Preclinical studies, along with early phase clinical trials, have examined antitumor properties of metformin on a variety of cancers. Metformin’s anticancer effects are well documented, demonstrating a great promise in improving current cancer therapies. However, there is a significant lack of late phase clinical trials, specifically those involving non-diabetic cancer patients, and therefore further research in this area is required.

scholarly journals Role of Unphosphorylated Transcription Factor STAT3 in Late Cerebral Ischemia after Subarachnoid Hemorrhage

2014 ◽  
Vol 34 (5) ◽  
pp. 759-763 ◽  
Author(s):  
Ajoy K Samraj ◽  
Anne H Müller ◽  
Anne-Sofie Grell ◽  
Lars Edvinsson
Keyword(s):  
Transcription Factor ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Molecular Mechanisms ◽  
Regulatory Molecule ◽  
Significant Enrichment ◽  
Binding Sequence ◽  
Transcription 3 ◽  
Transcription Factor Binding Sequence

Molecular mechanisms behind increased cerebral vasospasm and local inflammation in late cerebral ischemia after subarachnoid hemorrhage (SAH) are poorly elucidated. Using system biology tools and experimental SAH models, we have identified signal transducer and activator of transcription 3 (STAT3) transcription factor as a possible major regulatory molecule. On the basis of the presence of transcription factor binding sequence in the promoters of differentially regulated genes (significant enrichment PE: 6 × 105) and the consistent expression of STAT3 (mRNA, P = 0.0159 and Protein, P = 0.0467), we hypothesize that unphosphorylated STAT3 may directly DNA bind and probably affect the genes that are involved in inflammation and late cerebral ischemia to influence the pathologic progression of SAH.

scholarly journals Essential Role of STAT3 Signaling in Hair Follicle Homeostasis

2021 ◽  
Vol 12 ◽  
Author(s):  
Kosuke Miyauchi ◽  
Sewon Ki ◽  
Masao Ukai ◽  
Yoshie Suzuki ◽  
Kentaro Inoue ◽  
...  
Keyword(s):  
Hair Follicle ◽  
Inflammatory Responses ◽  
Expression Patterns ◽  
Critical Role ◽  
Dominant Negative ◽  
Cell Specification ◽  
Stat3 Signaling ◽  
Specific Pathogen ◽  
Transcription 3

Dominant-negative mutations associated with signal transducer and activator of transcription 3 (STAT3) signaling, which controls epithelial proliferation in various tissues, lead to atopic dermatitis in hyper IgE syndrome. This dermatitis is thought to be attributed to defects in STAT3 signaling in type 17 helper T cell　specification. However, the role of STAT3 signaling in skin epithelial cells remains unclear. We found that STAT3 signaling in keratinocytes is required to maintain skin homeostasis by negatively controlling the expression of hair follicle-specific keratin genes. These expression patterns correlated with the onset of dermatitis, which was observed in specific pathogen-free conditions but not in germ-free conditions, suggesting the involvement of Toll-like receptor-mediated inflammatory responses. Thus, our study suggests that STAT3-dependent gene expression in keratinocytes plays a critical role in maintaining the homeostasis of skin, which is constantly exposed to microorganisms.

scholarly journals Role of STAT3 in Cancer Metastasis and Translational Advances

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Mohammad Zahid Kamran ◽  
Prachi Patil ◽  
Rajiv P. Gude
Keyword(s):  
Cancer Metastasis ◽  
Cellular Proliferation ◽  
Nuclear Translocation ◽  
Signal Transducer ◽  
Surface Receptors ◽  
Physiological Conditions ◽  
Stat3 Signaling ◽  
Tumor Growth And Metastasis ◽  
Transcription 3

Signal transducer and activator of transcription 3 (STAT3) is a latent cytoplasmic transcription factor, originally discovered as a transducer of signal from cell surface receptors to the nucleus. It is activated by tyrosine phosphorylation at position 705 leading to its dimerization, nuclear translocation, DNA binding, and activation of gene transcription. Under normal physiological conditions, STAT3 activation is tightly regulated. However, compelling evidence suggests that STAT3 is constitutively activated in many cancers and plays a pivotal role in tumor growth and metastasis. It regulates cellular proliferation, invasion, migration, and angiogenesis that are critical for cancer metastasis. In this paper, we first describe the mechanism of STAT3 regulation followed by how STAT3 is involved in cancer metastasis, then we summarize the various small molecule inhibitors that inhibit STAT3 signaling.

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