ArticleCancer biology & therapy2018
Antidiabetic drugs influence molecular mechanisms in prostate cancer.
Article in Cancer biology & therapy, 2018. 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, 18 citations in OpenAlex.
- STAT3/LKB1 controls metastatic prostate cancer by regulating mTORC1/CREB pathway.Molecular cancer · 2023Article
- Systematic review of antitumour efficacy and mechanism of metformin activity in prostate cancer models.BJUI compass · 2023Review
- Synchronous Pancreatic Ductal Adenocarcinoma in the Head and Tail, a Double Trouble: A Case Report and Literature Review.Diagnostics (Basel, Switzerland) · 2022Article
- Precision intervention for prostate cancer: Re-evaluating who is at risk.Cancer letters · 2022Review
- Diabetes Mellitus and Pancreatic Ductal Adenocarcinoma-Prevalence, Clinicopathological Variables, and Clinical Outcomes.Cancers · 2022Article
- Is Metformin a Possible Beneficial Treatment for Psoriasis? A Scoping Review.Journal of personalized medicine · 2021Article
- Improvement Effect of Metformin on Female and Male Reproduction in Endocrine Pathologies and Its Mechanisms.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Association of type 2 diabetes mellitus and antidiabetic medication with risk of prostate cancer: a population-based case-control study.BMC cancer · 2020Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe investigated the role of diabetes mellitus (DM) and the molecular mechanisms of antidiabetic drugs in prostate cancer (PCa). PATIENTS AND
methods167 patients with both DM and PCa underwent radical prostatectomy (RPE). We divided our patient collective into "metformin" users, "insulin" users, "other antidiabetic drug" users and those with "no antidiabetic drug/diet only" (control group) and analyzed differences in PCa aggressiveness and laboratory parameters among treatment groups. In addition, we generated a tissue-micro-array (TMA) from RPE specimens for the analysis of candidate target pathways of antidiabetic drugs by immunohistochemistry (IHC).
resultsGleason score of both biopsy and RPE, biopsy undergrading, tumor stage as well as positive resection margins did not significantly change among groups. Preoperative body mass-index, PSA, fPSA and prostate volume/weight did not change among the treatment groups. As well, CRP, GOT, GPT, yGT, LDH, amylase, hemoglobin, TSH, FT3 and FT4 did not differ. Metformin or insulin use was not associated with changes in biochemical tumor recurrence or PCa specific mortality rates. However, tissue TMA analyses by IHC showed decreased mTOR activation, as indicated by phospho-mTOR in cancer tissue of patients with metformin and also with insulin use compared to the control group. In addition, we were able to show that the androgen receptor and the epithelial-cell contact marker E-cadherin decreased upon metformin use compared to the control group.
conclusionWe did not find a connection between antidiabetic drugs and PCa aggressiveness or progression. However, tumor biology seems to be different among patients with and without antidiabetic drugs.
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