Polychemotherapy with Curcumin and Doxorubicin via Biological Nanoplatforms: Enhancing Antitumor Activity DOI Creative Commons
Milad Ashrafizadeh, Ali Zarrabi,

Farid Hashemi

et al.

Pharmaceutics, Journal Year: 2020, Volume and Issue: 12(11), P. 1084 - 1084

Published: Nov. 11, 2020

Doxorubicin (DOX) is a well-known chemotherapeutic agent extensively applied in the field of cancer therapy. However, similar to other agents such as cisplatin, paclitaxel, docetaxel, etoposide and oxaliplatin, cells are able obtain chemoresistance that limits DOX efficacy. In respect dose-dependent side effect DOX, enhancing its dosage not recommended for effective chemotherapy. Therefore, different strategies have been considered reversing resistance diminishing effects. Phytochemical potential candidates this case due their great pharmacological activities. Curcumin antitumor phytochemical isolated from Curcuma longa with capacity suppressing metastasis proliferation affecting molecular pathways. Experiments demonstrated curcumin inhibiting by downregulating oncogene pathways MMP-2, TGF-β, EMT, PI3K/Akt, NF-κB AP-1. Furthermore, coadministration potentiates apoptosis induction cells. light this, nanoplatforms employed codelivery DOX. This results promoting bioavailability internalization aforementioned active compounds and, consequently, activity. Noteworthy, has reducing adverse effects on normal tissues via inflammation, oxidative stress apoptosis. The current review highlights anticancer mechanism, nanovehicles.

Language: Английский

Molecular Landscape of LncRNAs in Prostate Cancer: A focus on pathways and therapeutic targets for intervention DOI Creative Commons
Sepideh Mirzaei, Mahshid Deldar Abad Paskeh,

Elena Okina

et al.

Journal of Experimental & Clinical Cancer Research, Journal Year: 2022, Volume and Issue: 41(1)

Published: July 1, 2022

Abstract Background One of the most malignant tumors in men is prostate cancer that still incurable due to its heterogenous and progressive natures. Genetic epigenetic changes play significant roles development. The RNA molecules with more than 200 nucleotides length are known as lncRNAs these factors do not encode protein. They regulate gene expression at transcriptional, post-transcriptional levels. LncRNAs vital biological functions cells pathological events, hence their undergoes dysregulation. Aim review role alterations development emphasized here. Therefore, were chosen for this purpose level interaction other signaling networks progression examined. Key scientific concepts aberrant has been well-documented rate tumor regulated via affecting STAT3, NF-κB, Wnt, PI3K/Akt PTEN, among molecular pathways. Furthermore, radio-resistance chemo-resistance features cells. Overexpression tumor-promoting such HOXD-AS1 CCAT1 can result drug resistance. Besides, induce immune evasion upregulating PD-1. Pharmacological compounds quercetin curcumin have applied targeting lncRNAs. siRNA tool reduce thereby suppressing progression. Prognosis diagnosis clinical course be evaluated by exosomal lncRNA-p21 investigated serum patients a reliable biomarker.

Language: Английский

Citations

126

Cytoskeletal Dynamics in Epithelial-Mesenchymal Transition: Insights into Therapeutic Targets for Cancer Metastasis DOI Open Access
Arpita Datta, Shuo Deng, Vennila Gopal

et al.

Cancers, Journal Year: 2021, Volume and Issue: 13(8), P. 1882 - 1882

Published: April 14, 2021

In cancer cells, a vital cellular process during metastasis is the transformation of epithelial cells towards motile mesenchymal called to transition (EMT). The cytoskeleton an active network three intracellular filaments: actin cytoskeleton, microtubules, and intermediate filaments. These filaments play central role in structural design cell behavior are necessary for EMT. During EMT, undergo as manifested by elongation, migration, invasion, coordinated reorganization. extremely dynamic structure, controlled balance assembly disassembly Actin-binding proteins regulate polymerization depolymerization. Microtubule reorganization also plays important migration polarization. Intermediate rearranged, switching vimentin-rich network, this protein used marker cell. Hence, targeting EMT regulating activities their key components may be potential solution metastasis. This review summarizes research done on physiological functions its process, effect multidrug-resistant (MDR) cells—highlight some future perspectives therapy cytoskeleton.

Language: Английский

Citations

123

Mechanism of epithelial‐mesenchymal transition in cancer and its regulation by natural compounds DOI

Hui Li Ang,

Chakrabhavi Dhananjaya Mohan, Muthu K. Shanmugam

et al.

Medicinal Research Reviews, Journal Year: 2023, Volume and Issue: 43(4), P. 1141 - 1200

Published: March 17, 2023

Abstract Epithelial‐mesenchymal transition (EMT) is a complex process with primordial role in cellular transformation whereby an epithelial cell transforms and acquires mesenchymal phenotype. This plays pivotal tumor progression self‐renewal, exacerbates resistance to apoptosis chemotherapy. EMT can be initiated promoted by deregulated oncogenic signaling pathways, hypoxia, cells the microenvironment, resulting loss‐of‐epithelial polarity, cell–cell adhesion, enhanced invasive/migratory properties. Numerous transcriptional regulators, such as Snail, Slug, Twist, ZEB1/ZEB2 induce through downregulation of markers gain‐of‐expression markers. Additionally, cascades Wnt/β‐catenin, Notch, Sonic hedgehog, nuclear factor kappa B, receptor tyrosine kinases, PI3K/AKT/mTOR, Hippo, transforming growth factor‐β pathways regulate whereas they are often cancers leading aberrant EMT. Furthermore, noncoding RNAs, tumor‐derived exosomes, epigenetic alterations also involved modulation Therefore, regulation vital strategy control aggressive metastatic characteristics cells. Despite vast amount preclinical data on cancer progression, there lack clinical translation at therapeutic level. In this review, we have discussed thoroughly aforementioned transcription factors, RNAs (microRNAs, long RNA, circular RNA), modifications, exosomes cancers. We emphasized contribution drug possible interventions using plant‐derived natural products, their semi‐synthetic derivatives, nano‐formulations that described promising blockers.

Language: Английский

Citations

123

STAT3-EMT axis in tumors: Modulation of cancer metastasis, stemness and therapy response DOI
Mehrdokht Sadrkhanloo, Maliheh Entezari,

Sima Orouei

et al.

Pharmacological Research, Journal Year: 2022, Volume and Issue: 182, P. 106311 - 106311

Published: June 15, 2022

Language: Английский

Citations

115

Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response DOI Creative Commons
Milad Ashrafizadeh, Mahshid Deldar Abad Paskeh, Sepideh Mirzaei

et al.

Journal of Experimental & Clinical Cancer Research, Journal Year: 2022, Volume and Issue: 41(1)

Published: March 22, 2022

Abstract Prostate cancer is a leading cause of death worldwide and new estimates revealed prostate as the in men 2021. Therefore, strategies are pertinent treatment this malignant disease. Macroautophagy/autophagy “self-degradation” mechanism capable facilitating turnover long-lived toxic macromolecules organelles. Recently, attention has been drawn towards role autophagy how its modulation provides effective therapy. In present review, we provide mechanistic discussion cancer. Autophagy can promote/inhibit proliferation survival cells. Besides, metastasis cells affected (via induction inhibition) by autophagy. affect response to therapy such chemotherapy radiotherapy, given close association between apoptosis. Increasing evidence demonstrated that upstream mediators AMPK, non-coding RNAs, KLF5, MTOR others regulate Anti-tumor compounds, for instance phytochemicals, dually inhibit or induce For improving therapy, nanotherapeutics chitosan nanoparticles have developed. With respect context-dependent cancer, genetic tools siRNA CRISPR-Cas9 be utilized targeting autophagic genes. Finally, these findings translated into preclinical clinical studies improve prognosis patients. Graphical abstract

Language: Английский

Citations

111

Biological impact and therapeutic perspective of targeting PI3K/Akt signaling in hepatocellular carcinoma: Promises and Challenges DOI Creative Commons
Mahshid Deldar Abad Paskeh, Fatemeh Ghadyani, Mehrdad Hashemi

et al.

Pharmacological Research, Journal Year: 2022, Volume and Issue: 187, P. 106553 - 106553

Published: Nov. 16, 2022

Cancer progression results from activation of various signaling networks. Among these, PI3K/Akt contributes to proliferation, invasion, and inhibition apoptosis. Hepatocellular carcinoma (HCC) is a primary liver cancer with high incidence rate, especially in regions prevalence viral hepatitis infection. Autoimmune disorders, diabetes mellitus, obesity, alcohol consumption, inflammation can also lead initiation development HCC. The treatment HCC depends on the identification oncogenic factors that tumor cells develop resistance therapy. present review article focuses role progression. Activation promotes glucose uptake, favors glycolysis increases cell proliferation. It inhibits both apoptosis autophagy while promoting survival. stimulates epithelial-to-mesenchymal transition (EMT) matrix-metalloproteinase (MMP) expression during metastasis. In addition increasing colony formation capacity facilitating spread cells, angiogenesis. Therefore, silencing prevents aggressive behavior. confer drug resistance, particularly sorafenib, decreases radio-sensitivity cells. Anti-cancer agents, like phytochemicals small molecules suppress by limiting Being upregulated tissues clinical samples, be used as biomarker predict patients' response

Language: Английский

Citations

85

Non-coding RNA-based regulation of inflammation DOI
Milad Ashrafizadeh, Ali Zarrabi, Ebrahim Mostafavi

et al.

Seminars in Immunology, Journal Year: 2022, Volume and Issue: 59, P. 101606 - 101606

Published: Jan. 1, 2022

Language: Английский

Citations

71

The epithelial–mesenchymal plasticity landscape: principles of design and mechanisms of regulation DOI
Jef Haerinck, Steven Goossens, Geert Berx

et al.

Nature Reviews Genetics, Journal Year: 2023, Volume and Issue: 24(9), P. 590 - 609

Published: May 11, 2023

Language: Английский

Citations

71

Noncoding RNAs as regulators of STAT3 pathway in gastrointestinal cancers: Roles in cancer progression and therapeutic response DOI
Milad Ashrafizadeh, Chakrabhavi Dhananjaya Mohan, Shobith Rangappa

et al.

Medicinal Research Reviews, Journal Year: 2023, Volume and Issue: 43(5), P. 1263 - 1321

Published: March 23, 2023

Abstract Gastrointestinal (GI) tumors (cancers of the esophagus, gastric, liver, pancreas, colon, and rectum) contribute to a large number deaths worldwide. STAT3 is an oncogenic transcription factor that promotes genes associated with proliferation, antiapoptosis, survival, metastasis. overactivated in many human malignancies including GI which accelerates tumor progression, metastasis, drug resistance. Research recent years demonstrated noncoding RNAs (ncRNAs) play major role regulation signaling pathways pathway. The types endogenous ncRNAs are being extensively studied oncology microRNAs, long RNAs, circular RNAs. These can either be tumor‐promoters or tumor‐suppressors each one them imparts their activity via different mechanisms. pathway also tightly modulated by ncRNAs. In this article, we have elaborated on tumor‐promoting tumors. Subsequently, comprehensively discussed as well suppressor functions mechanism action known modulate cancers.

Language: Английский

Citations

64

MASLD and the Development of HCC: Pathogenesis and Therapeutic Challenges DOI Open Access

Anju Phoolchund,

Salim I. Khakoo

Cancers, Journal Year: 2024, Volume and Issue: 16(2), P. 259 - 259

Published: Jan. 6, 2024

Metabolic-dysfunction-associated steatotic liver disease (MASLD, previously known as non-alcoholic fatty (NAFLD)) represents a rapidly increasing cause of chronic and hepatocellular carcinoma (HCC), mirroring rates obesity metabolic syndrome in the Western world. MASLD-HCC can develop at an earlier stage fibrosis compared to other causes disease, presenting challenges how risk-stratify patients set up effective screening programmes. Therapeutic decision making for is also complicated by medical comorbidities presentation later stage. The response treatment, particularly immune checkpoint inhibitors, may vary aetiology and, future, patient stratification will be key optimizing therapeutic pathways.

Language: Английский

Citations

32