ArticleMolecular medicine reports2016
KiSS‑1‑mediated suppression of the invasive ability of human pancreatic carcinoma cells is not dependent on the level of KiSS‑1 receptor GPR54.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- The Role of Adipokines in Pancreatic Cancer.Frontiers in oncology · 2022Review
- Up-regulation of KISS1 as a novel target of Let-7i in melanoma serves as a potential suppressor of migration and proliferation in vitro.Journal of cellular and molecular medicine · 2021Article
- Reduced Kiss‑1 expression is associated with clinical aggressive feature of gastric cancer patients and promotes migration and invasion in gastric cancer cells.Oncology reports · 2020Observational
- Girdin interaction with vimentin induces EMT and promotes the growth and metastasis of pancreatic ductal adenocarcinoma.Oncology reports · 2020Article
- Role of the tumor microenvironment in regulating the anti-metastatic effect of KISS1.Clinical & experimental metastasis · 2020Review
- KISS1 in breast cancer progression and autophagy.Cancer metastasis reviews · 2019Review
- Overexpression of Collapsin Response Mediator Protein 1 Inhibits Human Trophoblast Cells Proliferation, Migration, and Invasion.Reproductive sciences (Thousand Oaks, Calif.) · 2019Article
- KISS1/KISS1R in Cancer: Friend or Foe?Frontiers in endocrinology · 2018Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The onset of local invasion and lymphatic metastasis in pancreatic cancer limits survival following surgical intervention and additional therapies. Reduced expression of KiSS‑1 in pancreatic cancer is associated with cancer metastasis. Previous studies have indicated that kisspeptin, the KiSS‑1 peptide, is able to bind to its receptor‑GPR54 (hOT7T175) and suppress the migration of PANC‑1 pancreatic cancer cells. Whether the metastatic suppression of KiSS‑1 is dependent on the levels of GPR54 in pancreatic cancer cell lines remains unclear. Human BxPC‑3 pancreatic carcinoma cells are highly differentiated without exhibiting metastasis, however PANC‑1 pancreatic carcinoma cells are poorly differentiated and exhibit local and lymph node metastasis. Compared with primary cultured trophoblasts, BxPc‑3 and PANC‑1 cells were observed to express low levels of KiSS‑1 mRNA and protein, measured using reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. However, greater mRNA and protein expression levels of GPR54 were observed in PANC‑1 cells compared with BxPc‑3 cells. An MTT assay was used to investigate the effect of KiSS‑1 on BxPc‑3 and PANC‑1 cell proliferation. There were no significant differences in proliferation following transfection with KiSS‑1 in BxPc‑3 and PANC‑1 cells compared with the controls (P>0.05). A Transwell assay with chambers coated with Matrigel was used to evaluate the in vitro invasive ability of BxPc‑3 and PANC‑1 cells, with the invasion index of BxPc‑3 and PANC‑1 cells significantly reduced following 48 h of KiSS‑1 overexpression (P<0.05). The mRNA and protein expression levels of KiSS‑1 were significantly increased in BxPc‑3 and PANC‑1 cells 48 h subsequent to transfection with KiSS‑1 (P<0.05), while GPR54 expression was not altered (P>0.05). KiSS‑1 is a metastasis suppressor gene of pancreatic cancer, and this suppression is not dependent on the expression levels of GPR54. Therefore, KiSS‑1 is potentially a novel target for gene therapy.
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