Role of protein S-Glutathionylation in cancer progression and development of resistance to anti-cancer drugs

2021 ◽  
Vol 704 ◽  
pp. 108890
Author(s):  
Debojyoti Pal ◽  
Archita Rai ◽  
Rahul Checker ◽  
R.S. Patwardhan ◽  
Babita Singh ◽  
...  
2018 ◽  
Vol 20 (1) ◽  
pp. 51 ◽  
Author(s):  
Yoojung Kwon ◽  
Youngmi Kim ◽  
Hyun Jung ◽  
Dooil Jeoung

Histone modification is associated with resistance to anti-cancer drugs. Epigenetic modifications of histones can regulate resistance to anti-cancer drugs. It has been reported that histone deacetylase 3 (HDAC3) regulates responses to anti-cancer drugs, angiogenic potential, and tumorigenic potential of cancer cells in association with cancer-associated genes (CAGE), and in particular, a cancer/testis antigen gene. In this paper, we report the roles of microRNAs that regulate the expression of HDAC3 and CAGE involved in resistance to anti-cancer drugs and associated mechanisms. In this review, roles of HDAC3-miRNAs-CAGE molecular networks in resistance to anti-cancer drugs, and the relevance of HDAC3 as a target for developing anti-cancer drugs are discussed.


2012 ◽  
Vol 32 (02) ◽  
pp. 95-104 ◽  
Author(s):  
C. Bokemeyer ◽  
F. Langer

SummaryCancer is characterized by bidirectional interrelations between tumour progression, coagulation activation, and inflammation. Tissue factor (TF), the principal initiator of the coagulation protease cascade, is centrally positioned in this complex triangular network due to its pleiotropic effects in haemostasis, angiogenesis, and haematogenous metastasis. While formation of macroscopic thrombi is the correlate of cancer-associated venous thromboembolism (VTE), a major healthcare burden in clinical haematology and oncology, microvascular thrombosis appears to be critically important to blood-borne tumour cell dissemination. In this regard, expression of TF in malignant tissues as well as shedding of TFbearing microparticles into the circulation are thought to be regulated by defined genetic events relevant to pathological cancer progression, thus directly linking Trousseau’s syndrome to molecular tumourigenesis.Because pharmacological inhibition of the TF pathway in selective tumour types and patient subgroups would be in line with the modern concept of individualized, targeted anti-cancer therapy, this review will focus on the role of TF in tumour biology and cancer-associated VTE.


2013 ◽  
Vol 41 (1) ◽  
pp. 293-298 ◽  
Author(s):  
Samireh Jorfi ◽  
Jameel M. Inal

Microvesicles are shed constitutively, or upon activation, from both normal and malignant cells. The process is dependent on an increase in cytosolic Ca2+, which activates different enzymes, resulting in depolymerization of the actin cytoskeleton and release of the vesicles. Drug resistance can be defined as the ability of cancer cells to survive exposure to a wide range of anti-cancer drugs, and anti-tumour chemotherapeutic treatments are often impaired by innate or acquired MDR (multidrug resistance). Microvesicles released upon chemotherapeutic agents prevent the drugs from reaching their targets and also mediate intercellular transport of MDR proteins.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Shao-Xing Dai ◽  
Wen-Xing Li ◽  
Fei-Fei Han ◽  
Yi-Cheng Guo ◽  
Jun-Juan Zheng ◽  
...  

Abstract There is a constant demand to develop new, effective, and affordable anti-cancer drugs. The traditional Chinese medicine (TCM) is a valuable and alternative resource for identifying novel anti-cancer agents. In this study, we aim to identify the anti-cancer compounds and plants from the TCM database by using cheminformatics. We first predicted 5278 anti-cancer compounds from TCM database. The top 346 compounds were highly potent active in the 60 cell lines test. Similarity analysis revealed that 75% of the 5278 compounds are highly similar to the approved anti-cancer drugs. Based on the predicted anti-cancer compounds, we identified 57 anti-cancer plants by activity enrichment. The identified plants are widely distributed in 46 genera and 28 families, which broadens the scope of the anti-cancer drug screening. Finally, we constructed a network of predicted anti-cancer plants and approved drugs based on the above results. The network highlighted the supportive role of the predicted plant in the development of anti-cancer drug and suggested different molecular anti-cancer mechanisms of the plants. Our study suggests that the predicted compounds and plants from TCM database offer an attractive starting point and a broader scope to mine for potential anti-cancer agents.


2015 ◽  
Vol 370 (1661) ◽  
pp. 20140039 ◽  
Author(s):  
Orest W. Blaschuk

The cell adhesion molecule (CAM), N-cadherin, has emerged as an important oncology therapeutic target. N-cadherin is a transmembrane glycoprotein mediating the formation and structural integrity of blood vessels. Its expression has also been documented in numerous types of poorly differentiated tumours. This CAM is involved in regulating the proliferation, survival, invasiveness and metastasis of cancer cells. Disruption of N-cadherin homophilic intercellular interactions using peptide or small molecule antagonists is a promising novel strategy for anti-cancer therapies. This review discusses: the discovery of N-cadherin, the mechanism by which N-cadherin promotes cell adhesion, the role of N-cadherin in blood vessel formation and maintenance, participation of N-cadherin in cancer progression, the different types of N-cadherin antagonists and the use of N-cadherin antagonists as anti-cancer drugs.


2006 ◽  
Vol 2 (4) ◽  
pp. 327-329 ◽  
Author(s):  
Ramzi Dagher ◽  
Richard Pazdur
Keyword(s):  

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 485 ◽  
Author(s):  
Marta Hałasa ◽  
Anna Wawruszak ◽  
Alicja Przybyszewska ◽  
Anna Jaruga ◽  
Małgorzata Guz ◽  
...  

Acetylation and deacetylation are posttranslational modifications (PTMs) which affect the regulation of chromatin structure and its remodeling. Acetylation of histone 3 at lysine placed on position 18 (H3K18Ac) plays an important role in driving progression of many types of cancer, including breast, colon, lung, hepatocellular, pancreatic, prostate, and thyroid cancer. The aim of this review is to analyze and discuss the newest findings regarding the role of H3K18Ac and acetylation of other histones in carcinogenesis. We summarize the level of H3K18Ac in different cancer cell lines and analyze its association with patients’ outcomes, including overall survival (OS), progression-free survival (PFS), and disease-free survival (DFS). Finally, we describe future perspectives of cancer therapeutic strategies based on H3K18 modifications.


2021 ◽  
Author(s):  
marjan hajimoradi javarsiani ◽  
javad sajedianfard ◽  
Shagayegh Haghjooy Javanmard ◽  
Micol Eleonora Fiori

Abstract Background Metformin has been the subject of recent studies aimed at the treatment of melanoma cancer. In this study, the anti-cancer effects of metformin, an antidiabetic drug, was investigated in-vitrousing the B16F10 melanoma cell line. Methods Melanoma cells were treated for 24 h with various concentrations of metformin, alone or incombination withdacarbazine. The effects of these two treatment agents on cell viability were evaluated by MTT assay. In addition, stemness and the activation of specific signaling pathways were evaluated by FACS and immunoblotting. Results Metformin induced β-catenin phosphorylation and decreasedmTOR and PARP expressions. Also, a normal dose of metformin was found toreducethe phosphorylation levels of4E-BP1, AKT, and S6rp.In this study, we evaluated the potential of metformin as a therapeutic agent against CSCs in the adjuvant setting. Conclusion Our data indicate that some transcriptional regulators and proteins in the above-mentioned pathwayswere associated with cancer progression and inhibited by adjuvant chemotherapy with metformin.Metformin significantly inhibited cell growth and proliferation pathways, including Wnt and PI3K/AKT/mTOR. These findings show the potential of metformin in cancer treatment.


Soft Matter ◽  
2015 ◽  
Vol 11 (21) ◽  
pp. 4173-4179 ◽  
Author(s):  
Debasish Saha ◽  
Fabienne Testard ◽  
Isabelle Grillo ◽  
Fatima Zouhiri ◽  
Didier Desmaele ◽  
...  

Squalene based nanoparticles obtained via nanoprecipitation are promising candidates as efficient anti-cancer drugs.


2019 ◽  
Vol 20 (10) ◽  
pp. 2519 ◽  
Author(s):  
Sheetal Parida ◽  
Sumit Siddharth ◽  
Dipali Sharma

Adiponectin is one of the most important adipocytokines secreted by adipocytes and is called a “guardian angel adipocytokine” owing to its unique biological functions. Adiponectin inversely correlates with body fat mass and visceral adiposity. Identified independently by four different research groups, adiponectin has multiple names; Acrp30, apM1, GBP28, and AdipoQ. Adiponectin mediates its biological functions via three known receptors, AdipoR1, AdipoR2, and T-cadherin, which are distributed throughout the body. Biological functions of adiponectin are multifold ranging from anti-diabetic, anti-atherogenic, anti-inflammatory to anti-cancer. Lower adiponectin levels have been associated with metabolic syndrome, type 2 diabetes, insulin resistance, cardiovascular diseases, and hypertension. A plethora of experimental evidence supports the role of obesity and increased adiposity in multiple cancers including breast, liver, pancreatic, prostrate, ovarian, and colorectal cancers. Obesity mediates its effect on cancer progression via dysregulation of adipocytokines including increased production of oncogenic adipokine leptin along with decreased production of adiponectin. Multiple studies have shown the protective role of adiponectin in obesity-associated diseases and cancer. Adiponectin modulates multiple signaling pathways to exert its physiological and protective functions. Many studies over the years have shown the beneficial effect of adiponectin in cancer regression and put forth various innovative ways to increase adiponectin levels.


Sign in / Sign up

Export Citation Format

Share Document