ArticleOncology letters2019
Upregulation of DLC-1 inhibits pancreatic cancer progression: Studies with clinical samples and a pancreatic cancer model.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 4 citations in OpenAlex.
- Characterization and validation of long noncoding RNAs as new candidates in prostate cancer.Cancer cell international · 2020Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deleted in liver cancer 1 (DLC-1) serves a vital role in the progression of multiple cancers, including those of the pancreas. Numerous studies have aimed to reveal the anti-cancer mechanisms of the DLC-1 gene, though few have focused on its impact on the development of pancreatic cancer. Using clinical pancreatic cancer samples and pancreatic cancer cell lines, the present study aimed to reveal the role of DLC-1 in this disease. The expression levels of DLC-1 were determined in pancreatic cancer and adjacent normal tissues from patients with pancreatic cancer, indicating a decreased expression level of DLC-1 in cancerous tissues. Using the pancreatic cancer cell line SW1990, the effect of DLC overexpression on cell proliferation, invasive capacity and the cell cycle and were assessed. Using a mouse tumor model, the tumor-progression capacity of transfected and untransfected SW1990 cells was investigated, indicating that DLC-1 transfection reduced the capacity for tumor progression. Thus, the present study indicated that the overexpression of DLC-1 inhibited the proliferation and reduced the invasive capacity of SW1990 cells both
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