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Intercellular TIMP-1-CD63 signaling directs the evolution of immune escape and metastasis in KRAS-mutated pancreatic cancer cells.
Mol Cancer
January 2025
Department of Physiology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Background And Aims: Oncogenic KRAS mutations are present in approximately 90% of pancreatic ductal adenocarcinoma (PDAC). However, Kras mutation alone is insufficient to transform precancerous cells into metastatic PDAC. This study investigates how KRAS-mutated epithelial cells acquire the capacity to escape senescence or even immune clearance, thereby progressing to advanced PDAC.
View Article and Find Full Text PDFKnockdown of CNOT3, a subunit of the CCR4-NOT deadenylase complex, sensitizes A549 human non-small cell lung cancer cells to senescence-inducing stimuli.
Biochem Biophys Res Commun
January 2025
Membranology Unit, Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha, Onna, Okinawa, 904-0495, Japan. Electronic address:
Cellular senescence is an essentially irreversible cell cycle arrest associated with upregulated inflammatory responses that contribute to various pathological and physiological processes, including aging, cancer, and cancer prevention. However, the underlying mechanisms are not fully understood. Here, we show that the downregulation of CNOT3, a subunit of the CCR4-NOT complex that deadenylates mRNA poly(A) tails, promotes cellular senescence in subpopulation of A549 human non-small cell lung cancer cells.
View Article and Find Full Text PDFNanosize Non-Viral Gene Therapy Reverses Senescence Reprograming Driven by PBRM1 Deficiency to Suppress iCCA Progression.
Adv Sci (Weinh)
January 2025
Department of Hepatic Surgery, Center of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, 510080, China.
Polybromo-1 (PBRM1) serves as a crucial regulator of gene transcription in various tumors, including intrahepatic cholangiocarcinoma (iCCA). However, the exact role of PBRM1 in iCCA and the mechanism by which it regulates downstream target genes remain unclear. This research has revealed that PBRM1 is significantly downregulated in iCCA tissues, and this reduced expression is linked to aggressive clinicopathological features and a poor prognosis.
View Article and Find Full Text PDFp21 as an essential regulator of neurogenic homeostasis in neuropathological conditions.
Neural Regen Res
January 2025
Institute of Biochemistry and Cell Biology, IBBC, CNR, Monterotondo, Rome, Italy.
Anti-proteolytic regulation of KRAS by USP9X/NDRG3 in KRAS-driven cancer development.
Nat Commun
January 2025
Personalized Genomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea.
Cancers with activating mutations of KRAS show a high prevalence but remain intractable, requiring innovative strategies to overcome the poor targetability of KRAS. Here, we report that KRAS expression is post-translationally up-regulated through deubiquitination when the scaffolding function of NDRG3 (N-Myc downstream-regulated gene 3) promotes specific interaction between KRAS and a deubiquitinating enzyme, USP9X. In KRAS-mutant cancer cells KRAS protein expression, downstream signaling, and cell growth are highly dependent on NDRG3.
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