Results 61 to 70 of about 3,125,328 (279)

microRNAs Associated with Gemcitabine Resistance via EMT, TME, and Drug Metabolism in Pancreatic Cancer

open access: yesCancers, 2023
Simple Summary We herein reviewed the current evidence for the role of microRNAs (miRNAs) in the mechanism of chemoresistance in pancreatic cancer.
N. Funamizu   +5 more
semanticscholar   +1 more source

A kinome screen identifies checkpoint kinase 1 (CHK1) as a sensitizer for RRM1-dependent gemcitabine efficacy. [PDF]

open access: yesPLoS ONE, 2013
Gemcitabine is among the most efficacious and widely used antimetabolite agents. Its molecular targets are ribonucleotide reductase M1 (RRM1) and elongating DNA.
Jun Zhou   +6 more
doaj   +1 more source

Cancer-Associated Fibroblasts Confer Gemcitabine Resistance to Pancreatic Cancer Cells through PTEN-Targeting miRNAs in Exosomes

open access: yesCancers, 2022
Simple Summary Previous studies have shown that cancer associated fibroblasts exposed to chemotherapy release exosomes which promote chemoresistance in recipient cells.
Katherine E. Richards   +3 more
semanticscholar   +1 more source

Human concentrative nucleoside transporter 3 transfection with ultrasound and microbubbles in nucleoside transport deficient HEK293 cells greatly increases gemcitabine uptake. [PDF]

open access: yesPLoS ONE, 2013
Gemcitabine is a hydrophilic clinical anticancer drug that requires nucleoside transporters to cross plasma membranes and enter cells. Pancreatic adenocarcinomas with low levels of nucleoside transporters are generally resistant to gemcitabine and are ...
Robert J Paproski   +6 more
doaj   +1 more source

Resistance to Gemcitabine in Pancreatic Cancer Is Connected to Methylglyoxal Stress and Heat Shock Response

open access: yesCells, 2023
Pancreatic ductal adenocarcinoma (PDAC) is a fatal disease with poor prognosis. Gemcitabine is the first-line therapy for PDAC, but gemcitabine resistance is a major impediment to achieving satisfactory clinical outcomes.
Rebekah Crake   +14 more
doaj   +1 more source

N6-methyladenosine modified TGFB2 triggers lipid metabolism reprogramming to confer pancreatic ductal adenocarcinoma gemcitabine resistance

open access: yesOncogene
Gemcitabine resistance is a major obstacle to the effectiveness of chemotherapy in pancreatic ductal adenocarcinoma (PDAC). Therefore, new strategies are needed to sensitize cancer cells to gemcitabine.
Ming-Jian Ma   +11 more
semanticscholar   +1 more source

Gemcitabine resistance of pancreatic cancer cells is mediated by IGF1R dependent upregulation of CD44 expression and isoform switching

open access: yesCell Death and Disease, 2022
Chemoresistance in pancreatic cancer cells may be caused by the expansion of inherently resistant cancer cells or by the adaptive plasticity of initially sensitive cancer cells.
Chen Chen   +6 more
semanticscholar   +1 more source

LncRNA MACC1-AS1 induces gemcitabine resistance in pancreatic cancer cells through suppressing ferroptosis

open access: yesCell Death Discovery
Pancreatic ductal adenocarcinoma (PDA) mortality is primarily attributed to metastasis and chemotherapy resistance. In this research, the long non-coding RNA MACC1-AS1 was studied, playing a significant role in regulating lipid oxidation processes.
Jiyun Zhu   +9 more
semanticscholar   +1 more source

Integrative Genomic Analysis of Gemcitabine Resistance in Pancreatic Cancer by Patient-derived Xenograft Models

open access: yesClinical Cancer Research, 2021
Purpose: Gemcitabine is most commonly used for pancreatic cancer. However, the molecular features and mechanisms of the frequently occurring resistance remain unclear.
Gang Yang   +13 more
semanticscholar   +1 more source

Therapeutic strategies for MMAE‐resistant bladder cancer through DPP4 inhibition

open access: yesMolecular Oncology, EarlyView.
We established monomethyl auristatin E (MMAE)‐resistant bladder cancer (BC) cell lines by exposure to progressively increasing concentrations of MMAE in vitro. RNA sequencing showed DPP4 expression was increased in MMAE‐resistant BC cells. Both si‐DPP4 and the DPP4 inhibitor sitagliptin suppressed the viability of MMAE‐resistant BC cells.
Gang Li   +10 more
wiley   +1 more source

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