Evidence map›Paper›PMID 25228112›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2015

TGF-β1 mediates the radiation response of prostate cancer.

Chun-Te Wu, Ching-Chuan Hsieh, Tzu-Chen Yen, Wen-Cheng Chen, Miao-Fen Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  6. Article
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  12. Radiotherapy combined with immunotherapy: the dawn of cancer treatment.Signal transduction and targeted therapy · 2022
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Loss of GTPase of immunity-associated protein 5 (Gimap5) promotes pathogenic CD4The Journal of allergy and clinical immunology · 2019
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Chun-Te WuDepartment of Urology, Chang Gung Memorial Hospital, KeeLung, Taiwan.
Ching-Chuan Hsieh
Tzu-Chen Yen
Wen-Cheng Chen
Miao-Fen Chen
Chang Gung University · TWChiayi Chang Gung Memorial Hospital · TWMemorial Hospital of South Bend · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledRadiotherapy is the main treatment modality for prostate cancer. This study investigated the role of TGF-β1 in biological sequelae and tumor regrowth following irradiation, which are critical for the clinical radiation response of prostate cancer. Human and murine prostate cancer cell lines, and corresponding hormone-refractory (HR) cells, were used to examine the radiation response by clonogenic assays in vitro and tumor growth delay in vivo. Biological changes after irradiation, including cell death and tumor regrowth, were examined by experimental manipulation of TGF-β1 signaling. The correlations among tumor radiation responses, TGF-β1 levels, and regulatory T cells (Tregs) recruitment were also evaluated using animal experiments. HR prostate cancer cells appeared more radioresistant and had higher expression of TGF-β1 compared to hormone-sensitive (HS) cells. TGF-β1 expression was positively linked to irradiation and radioresistance, as demonstrated by in vitro and in vivo experiments. Inhibition of TGF-β1 increased tumor inhibition and DNA damage after irradiation. When mice were irradiated with a sub-lethal dose, the regrowth of irradiated tumors was significantly correlated with TGF-β1 levels and Tregs accumulation in vivo. Furthermore, blocking TGF-β1 clearly attenuated Tregs accumulation and tumor regrowth following treatment. These data demonstrate that TGF-β1 is important in determining the radiation response of prostate cancer, including tumor cell killing and the tumor microenvironment. Therefore, concurrent treatment with a TGF-β1 inhibitor is a potential therapeutic strategy for increasing the radiation response of prostate cancer, particularly for more aggressive or HR cancer cells. KEY MESSAGE: • HR prostate cancer cells appeared more radioresistant and had higher expression of TGF-β1. • TGF-β1 was positively linked to the radiation resistance of prostate cancer. • Tumor regrowth following irradiation was significantly correlated with TGF-β1 and Tregs levels. • Blocking TGF-β1 significantly attenuated RT-induced DNA repair and Tregs. • TGF-β1 inhibitor increases the radiation response of HR cancer cells.

Indexed as

AnimalsCell Line, TumorHumansMaleMiceMice, Inbred C57BLMice, NudeProstatic NeoplasmsT-Lymphocytes, RegulatoryTransforming Growth Factor beta1Transforming Growth Factor beta1

Identifiers

PMID25228112
OpenAlexW2054463613

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.