Pancreatic cancer is a common malignant tumor worldwide. Extensive studies have been conducted on the functional role of long noncoding RNAs in pancreatic cancer. In this study, long intergenic nonprotein coding RNA 173 (LINC00173) was highly expressed in pancreatic cancer tissues. functional experiments showed that LINC00173 overexpression inhibited the proliferation and invasion of pancreatic cancer cells and promoted cell apoptosis in MIA PaCa-2 and PANC-1 cells. RNA sequencing analysis and Western blot assays demonstrated that LINC00173 reduced the expression of sphingosine kinase 1 (SPHK1) and then inhibited the protein expression of activated phospho-protein kinase B (AKT) and NF-κB. functional assays also revealed that LINC00173 inhibited the growth of pancreatic cancer xenografts, repressed cell proliferation, promoted cell apoptosis, and inhibited SPHK1 expression. The combined results of this study indicate that LINC00173 inhibits pancreatic cancer progression by repressing SPHK1 expression. Improving LINC00173 may represent a therapeutic strategy for pancreatic cancer in the future.
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http://dx.doi.org/10.1089/dna.2020.6103 | DOI Listing |
JCO Clin Cancer Inform
January 2025
Machine Learning Department, H. Lee Moffit Cancer Center and Research Institute, Tampa, FL.
Purpose: Adaptive radiotherapy accounts for interfractional anatomic changes. We hypothesize that changes in the gross tumor volumes identified during daily scans could be analyzed using delta-radiomics to predict disease progression events. We evaluated whether an auxiliary data set could improve prediction performance.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Radiation Oncology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China.
Background: The role of adjuvant radiotherapy in pancreatic cancer following radical surgery remains a subject of of controversy. This study aimed to more accurately screen pancreatic patients who benefit from adjuvant radiotherapy.
Methods: Clinicopathologic characteristics of patients with resectable pancreatic cancer were collected from the Surveillance, Epidemiology, and End Results (SEER) database (2004-2015).
PLoS One
January 2025
Cardiovascular Outcomes Research Laboratories (CORELAB), University of California, Los Angeles, Los Angeles, CA, United States of America.
Purpose: Patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) have been noted to face increased cancer incidence. Yet, the impact of concomitant renal dysfunction on acute outcomes following elective surgery for cancer remains to be elucidated.
Methods: All adult hospitalizations entailing elective resection for lung, esophageal, gastric, pancreatic, hepatic, or colon cancer were identified in the 2016-2020 National Inpatient Sample.
Cancer Res
January 2025
Tsinghua University, Beijing, China.
Pancreatic ductal adenocarcinoma (PDAC) is highly aggressive and lacks effective therapeutic options. Cancer cells frequently become more dependent on splicing factors than normal cells due to increased rates of transcription. Terminal uridylyltransferase 1 (TUT1) is a specific terminal uridylyltransferase for U6 small nuclear RNA (snRNA), which plays a catalytic role in the spliceosome.
View Article and Find Full Text PDFCell Rep
January 2025
MOE Key Laboratory of Biosystems Homeostasis & Protection, and Zhejiang Provincial Key Laboratory of Cancer Molecular Cell Biology, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang 310058, China; Center for Life Sciences, Shaoxing Institute, Zhejiang University, Shaoxing, Zhejiang 321000, China; Cancer Center, Zhejiang University, Hangzhou, Zhejiang 310058, China; The Second Affiliated Hospital, Zhejiang University, Hangzhou, Zhejiang 310009, China. Electronic address:
Transforming growth factor β (TGF-β) is well known to play paradoxical roles in tumorigenesis as it has both growth-inhibitory and pro-metastatic effects. However, the underlying mechanisms of how TGF-β drives the opposing responses remain largely unknown. Here, we report that ERBB4, a member of the ERBB receptor tyrosine kinase family, specifically promotes TGF-β's metastatic response but not its anti-growth response.
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