Interplay between endoplasmic reticulum stress and non-coding RNAs in cancer

Journal of Hematology & Oncology, Journal Year: 2020, Volume and Issue: 13(1)

Published: Dec. 1, 2020

Abstract To survive, cancer cells are subjected to various internal and external adverse factors, including genetic mutations, hypoxia, nutritional deficiencies, drug toxicity. All of these factors result in the accumulation unfolded proteins endoplasmic reticulum, which leads a condition termed reticulum stress (ER stress) triggers protein response (UPR). UPR downstream components strictly control transcription translation reprogramming ensure selective gene expression, that non-coding RNA (ncRNAs), adapt environments. NcRNAs, microRNAs (miRNAs), long RNAs (lncRNAs), circular (circRNAs), play important roles regulating target expression translation, their aberrant is related tumor development. Dysregulation ncRNAs involved regulation cellular characteristics cells, growth, apoptosis, metastasis, angiogenesis, sensitivity, stem cell properties. Notably, ER can regulate each other collaborate determine fate cells. Therefore, investigating interaction between crucial for developing effective treatment prevention strategies. In this review, we summarize stress-triggered signaling pathways carcinogenesis followed by mutual cancer, provide further insights into understanding tumorigenesis therapeutic

Language: Английский

---

Exploring the Roles of lncRNAs in GBM Pathophysiology and Their Therapeutic Potential

Cells, Journal Year: 2020, Volume and Issue: 9(11), P. 2369 - 2369

Published: Oct. 28, 2020

Glioblastoma (GBM) remains the most devastating primary central nervous system malignancy with a median survival of around 15 months. The past decades research have not yielded significant advancements in treatment GBM. In that same time, novel class molecules, long non-coding RNAs (lncRNAs), has been found to play multitude roles cancer and normal biology. increased accessibility next generation sequencing technologies advent lncRNA-specific microarrays facilitated study lncRNA etiology. Molecular computational methods can be applied predict function. LncRNAs serve as molecular decoys, scaffolds, super-enhancers, or repressors. These molecules phenotypic switches for GBM cells at expression and/or epigenetic levels. affect stemness/differentiation, proliferation, invasion, survival, DNA damage response, chromatin dynamics. Aberrant these transcripts may facilitate therapy resistance, leading tumor recurrence. could theragnostic prognostic biomarkers other cancers. RNA-based therapeutics also employed target lncRNAs route recurrent this review, we explore pathophysiology posit their therapeutic potential

Language: Английский

---

m6A-induced LINC00958 promotes breast cancer tumorigenesis via the miR-378a-3p/YY1 axis

Cell Death Discovery, Journal Year: 2021, Volume and Issue: 7(1)

Published: Feb. 2, 2021

Abstract Increasing evidence demonstrates that long noncoding RNAs (lncRNAs) play critical roles in human breast cancer (BC) tumorigenesis. However, the mechanisms by which lncRNA and N 6 -methyladenosine (m A) regulate BC tumorigenesis are still unclear. In present research, LINC00958 was markedly overexpressed tissue cells, upregulation promoted tumor progression of cells. Mechanistically, m A methyltransferase-like 3 (METTL3) gave rise to promoting its RNA transcript stability. Moreover, acted as a competitive endogenous for miR-378a-3p promote YY1. Overall, these data provide novel insight into how A-mediated regulates

Language: Английский

---

PDIA3P1 promotes Temozolomide resistance in glioblastoma by inhibiting C/EBPβ degradation to facilitate proneural-to-mesenchymal transition

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

Published: July 15, 2022

Resistance to temozolomide (TMZ) is a major obstacle preventing glioblastoma (GBM) recurrence after surgery. Although long noncoding RNAs (lncRNAs) play variety of roles in GBM, the lncRNAs that regulate TMZ resistance have not yet been clearly elucidated. This study aims identify may affect treatment sensitivity and explore novel therapeutic strategies overcome GBM.LncRNAs associated with were identified using Cancer Cell Line Encyclopedia (CCLE) Genomics Drug Sensitivity (GDSC) datasets. Quantitative real-time PCR (qRT-PCR) was used determine expression PDIA3P1 TMZ-resistant TMZ-sensitive GBM cell lines. Both gain-of-function loss-of-function studies assess effects on vitro vivo assays. Glioma stem cells (GSCs) effect subtype. The hypothesis promotes proneural-to-mesenchymal transition (PMT) established bioinformatics analysis functional experiments. RNA pull-down immunoprecipitation (RIP) assays performed examine interaction between C/EBPβ. posttranslational modification mechanism C/EBPβ verified ubiquitination coimmunoprecipitation (co-IP) CompuSyn leveraged calculate combination index (CI), antitumor combined nefllamapimod (NEF) validated both vivo.We lncRNA, PDIA3P1, which upregulated Overexpression promoted acquisition resistance, whereas knockdown restored sensitivity. MES-GBM, PMT progression GSCs, caused GBMs be more resistant treatment. Mechanistically, disrupted C/EBPβ-MDM2 complex stabilized protein by MDM2-mediated ubiquitination. Expression time- concentration-dependent manner response treatment, TMZ-induced upregulation mediated p38α-MAPK signaling pathway. NEF small molecule drug specifically targets p38α excellent blood-brain barrier (BBB) permeability. blocked TMZ-responsive produced synergistic when at specific concentrations. exhibited vivo.PDIA3P1 stabilizing C/EBPβ, reducing inhibits upregulation, provides better effects.

Language: Английский

---

The CTCF/LncRNA‐PACERR complex recruits E1A binding protein p300 to induce pro‐tumour macrophages in pancreatic ductal adenocarcinoma via directly regulating PTGS2 expression

Clinical and Translational Medicine, Journal Year: 2022, Volume and Issue: 12(2)

Published: Feb. 1, 2022

Language: Английский

---