Unveiling the connection: Long-chain non-coding RNAs and critical signaling pathways in breast cancer

Pathology - Research and Practice, Journal Year: 2023, Volume and Issue: 249, P. 154736 - 154736

Published: Aug. 3, 2023

Language: Английский

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SOX2 function in cancers: Association with growth, invasion, stemness and therapy response

Biomedicine & Pharmacotherapy, Journal Year: 2022, Volume and Issue: 156, P. 113860 - 113860

Published: Oct. 20, 2022

Language: Английский

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m⁶A‐Dependent Modulation via IGF2BP3/MCM5/Notch Axis Promotes Partial EMT and LUAD Metastasis

Advanced Science, Journal Year: 2023, Volume and Issue: 10(20)

Published: May 12, 2023

The importance of mRNA N6-methyladenosine (m6 A) modification during tumor metastasis is controversial as it plays distinct roles in different biological contexts. Moreover, how cancer cell plasticity shaped by m6 A interesting but remains uncharacterized. Here, this work shows that reader insulin like growth factor 2 binding protein 3 (IGF2BP3) remarkably upregulated metastatic lung adenocarcinoma (LUAD) and indicates worse prognosis patients. Interestingly, IGF2BP3 induces partial epithelial-mesenchymal-transition (EMT) confers LUAD cells to metastasize through A-dependent overactivation Notch signaling. Mechanistically, recognized A-modified minichromosome maintenance complex component (MCM5) mRNAs prolong stability them, subsequently upregulating MCM5 protein, which competitively inhibits SIRT1-mediated deacetylation Notch1 intracellular domain (NICD1), stabilizes NICD1 contributes IGF2BP3-mediated cellular plasticity. Notably, a tight correlation the IGF2BP3/MCM5/Notch axis evidenced clinical specimens. Therefore, study elucidates critical role on fostering via above axis, providing potential targets for LUAD.

Language: Английский

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Emerging roles of endoplasmic reticulum stress in the cellular plasticity of cancer cells

Frontiers in Oncology, Journal Year: 2023, Volume and Issue: 13

Published: Feb. 20, 2023

Cellular plasticity is a well-known dynamic feature of tumor cells that endows tumors with heterogeneity and therapeutic resistance alters their invasion-metastasis progression, stemness, drug sensitivity, thereby posing major challenge to cancer therapy. It becoming increasingly clear endoplasmic reticulum (ER) stress hallmark cancer. The dysregulated expression ER sensors the activation downstream signaling pathways play role in regulation progression cellular response various challenges. Moreover, mounting evidence implicates cell plasticity, including epithelial-mesenchymal phenotype, stem vasculogenic mimicry phenotype plasticity. influences several malignant characteristics cells, epithelial-to-mesenchymal transition (EMT), maintenance, angiogenic function, sensitivity targeted emerging links between are implicated chemoresistance discussed this review, which may aid formulating strategies target anticancer treatments.

Language: Английский

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Understanding the Complex Milieu of Epithelial-Mesenchymal Transition in Cancer Metastasis: New Insight Into the Roles of Transcription Factors

Frontiers in Oncology, Journal Year: 2021, Volume and Issue: 11

Published: Nov. 18, 2021

Epithelial-mesenchymal transition (EMT) is a physiological program during which polarised, immobile epithelial cells lose connection with their neighbours and are converted to migratory mesenchymal phenotype. Mechanistically, EMT occurs

Language: Английский

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Progress of tumor-associated macrophages in the epithelial-mesenchymal transition of tumor

Frontiers in Oncology, Journal Year: 2022, Volume and Issue: 12

Published: July 28, 2022

As a significant public health problem with high morbidity and mortality worldwide, tumor is one of the major diseases endangering human life. Moreover, metastasis most important contributor to death patients. Epithelial-mesenchymal transition (EMT) an essential biological process in developing primary tumors metastasis. It underlies progression by inducing series alterations cells that confer ability move migrate. Tumor-associated macrophages (TAMs) are infiltrating immune microenvironment, they play indispensable role EMT interacting cells. With increasing clarity relationship between TAMs metastasis, targeting processes emerging as promising target for new cancer therapies. Therefore, this paper reviews recent research progress tumor-associated epithelial-mesenchymal briefly discusses current anti-tumor therapies processes.

Language: Английский

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MiR-455-5p suppresses PDZK1IP1 to promote the motility of oral squamous cell carcinoma and accelerate clinical cancer invasion by regulating partial epithelial-to-mesenchymal transition

Journal of Experimental & Clinical Cancer Research, Journal Year: 2023, Volume and Issue: 42(1)

Published: Feb. 3, 2023

Lymph node and distant metastasis contribute to poor outcomes in patients with oral squamous cell carcinoma (OSCC). The mechanisms regulating cancer migration invasion play a key role OSCC.We determined ability of OSCC by wound-healing assay, two-chamber transwell assay mobility tracking evaluated tumor vivo. Western blot (WB), qRT-PCR, RNA-seq, dual-luciferase reporter assays nuclear/cytoplasmic fractionation were performed investigate the potential mechanism. Immunohistochimical (IHC) staining vimentin PDZK1IP1 expression tissues.In this study, we that miR-455-5p was associated lymph clinical invasion, leading OSCC. MiR-455-5p promoted induced epithelial-to-mesenchymal transition (EMT). We also identified new biomarker, (MAP17), targeted miR-455-5p. knockdown led migration, metastasis, EMT, increased transforming growth factor-β signaling In addition, overexpression inhibition collective migration. According data from Cancer Genome Atlas database NCKU-OrCA-40TN set, are positively negatively correlated, respectively, partial EMT score. High high levels low MAP17 H-scores. had higher rates disease recurrence than did expression, especially for risk factors expression. These results suggest suppresses mediates progression. may therefore serve as biomarkers be involved cells. an independent factor impacts recurrence.

Language: Английский

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SPINKs in Tumors: Potential Therapeutic Targets

Frontiers in Oncology, Journal Year: 2022, Volume and Issue: 12

Published: Feb. 11, 2022

The serine protease inhibitor Kazal type (SPINK) family includes SPINK1-14 and is the largest branch in family. SPINKs play an important role pancreatic physiology disease, sperm maturation capacitation, Nager syndrome, inflammation skin barrier. Evidence shows that unregulated expression of SPINK1, 2, 4, 5, 6, 7, 13 closely related to human tumors. Different exhibit various regulatory modes different tumors can be used as tumor prognostic markers. This article reviews cancer processes helps identify new treatment targets.

Language: Английский

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Prognostic and Clinicopathological Significance of the Aberrant Expression of β-Catenin in Oral Squamous Cell Carcinoma: A Systematic Review and Meta-Analysis

Cancers, Journal Year: 2022, Volume and Issue: 14(3), P. 479 - 479

Published: Jan. 18, 2022

This systematic review and meta-analysis aims to evaluate the prognostic clinicopathological significance of aberrant expression β-catenin (assessed through immunohistochemical loss membrane expression, cytoplasmic nuclear expression) in oral squamous cell carcinoma (OSCC). We searched for primary-level studies published before October-2021 PubMed, Embase, Web Science, Scopus, Google Scholar, with no limitation regard their publication date or language. evaluated methodological quality risk bias included using QUIPS tool, carried out meta-analyses, explored heterogeneity sources across subgroups meta-regression, conducted sensitivity small-study effects analyses. Forty-one (2746 patients) met inclusion criteria. The was statistically associated poor overall survival (HR = 1.77, 95% CI 1.20–2.60, p 0.004), disease-free 2.44, 1.10–5.50, 0.03), N+ status (OR 2.39, 1.68–3.40, < 0.001), higher clinical stage 2.40, 1.58–3.63, tumour size 1.76, 1.23–2.53, moderately-poorly differentiated OSCC 1.57, 1.09–2.25, 0.02). showed largest effect most meta-analyses (singularly [HR 2.37, 1.55–3.62, 0.001], [OR 3.44, 2.40–4.93, 0.001] 2.51, 1.17–5.35, 0.02]). In conclusion, our findings indicate that assessment could be incorporated as an additional complementary routine biomarker patients OSCC.

Language: Английский

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HIV-1 Tat-induced disruption of epithelial junctions and epithelial-mesenchymal transition of oral and genital epithelial cells lead to increased invasiveness of neoplastic cells and the spread of herpes simplex virus and cytomegalovirus

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: Feb. 13, 2025

Human immunodeficiency virus (HIV-1) transactivator Tat is a unique multi-functional viral protein secreted by infected cells. Although its primary function to promote HIV-1 transcription, interacts with neighboring cells and induces numerous disease-associated pathological changes. Despite the substantial reduction of load disease burden, expression secretion persist in people living HIV who are undergoing treatment highly effective combination antiretroviral therapy (cART). both oral genital epithelial impairs their mucosal barrier functions, which facilitates entry other pathogenic viruses. Tat-mediated interactions human papillomavirus (HPV) -infected HPV-negative neoplastic lead epithelial-mesenchymal transition increased invasiveness malignant Likewise, Tat-induced disruption cell junctions leads herpes simplex virus-1 (HSV-1) infection spread via exposure receptor, nectin-1. cytomegalovirus (HCMV) activating mitogen-activated kinases (MAPK) promoting NF-κB signaling, critical for replication production progeny virions. extracellular also plays role herpesvirus 8 (HHV8) -caused Kaposi sarcoma (KS) pathogenesis synergizing HHV-8 lytic proteins proliferation, angiogenesis, migration endothelial Collectively, these findings emphasize impact on HIV/AIDS during cART era highlight need further research molecular mechanisms underlying

Language: Английский

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