Evidence map›Paper›PMID 35361751›Full record

ArticleCell death & disease2022

AMTB, a TRPM8 antagonist, suppresses growth and metastasis of osteosarcoma through repressing the TGFβ signaling pathway.

Yujie Liu, Ao Leng, Lin Li, Bo Yang, Shihui Shen, Hui Chen, Enhao Zhu, Qiyue Xu, Xiaoyu Ma, Peilin Shi and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  8. Role of TRP Channels in Cancer-Induced Bone Pain.International journal of molecular sciences · 2025
    Review
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  10. Article
  11. Review
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  15. Targeting Grancalcin Accelerates Wound Healing by Improving Angiogenesis in Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  16. Article
  17. Article
  18. Review
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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

16 authors at 2 institutions in 1 country.

Yujie Liu *Department of Orthorpedics,Department of Orthopedic Oncology and Spine Tumor Center, Changzheng Hospital, Navy Medical University, Shanghai, China.ORCID 0000-0002-9303-8192
Ao Leng *Department of Orthorpedics,Department of Orthopedic Oncology and Spine Tumor Center, Changzheng Hospital, Navy Medical University, Shanghai, China.
Lin Li *Department of Orthorpedics,Department of Orthopedic Oncology and Spine Tumor Center, Changzheng Hospital, Navy Medical University, Shanghai, China.
Bo YangShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
Shihui ShenShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
Hui ChenShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
Enhao ZhuShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
Qiyue XuShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
Xiaoyu MaDepartment of Orthorpedics,Department of Orthopedic Oncology and Spine Tumor Center, Changzheng Hospital, Navy Medical University, Shanghai, China.
Peilin ShiShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
Yun LiuShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
Tielong LiuDepartment of Orthorpedics,Department of Orthopedic Oncology and Spine Tumor Center, Changzheng Hospital, Navy Medical University, Shanghai, China.
Lei LiShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
Kun LiShanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China. kunli12345@163.com.ORCID 0000-0002-5863-9865
Dan ZhangDepartment of Orthorpedics,Department of Orthopedic Oncology and Spine Tumor Center, Changzheng Hospital, Navy Medical University, Shanghai, China. zhangadanbama@hotmail.com.ORCID 0000-0001-9055-1954
Jianru XiaoDepartment of Orthorpedics,Department of Orthopedic Oncology and Spine Tumor Center, Changzheng Hospital, Navy Medical University, Shanghai, China. jianruxiao83@163.com.ORCID 0000-0001-5409-6245
Shanghai Changzheng Hospital · CNEast China Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since its first identification in prostate cancers and prostate tissues, transient receptor potential melastatin-subfamily member 8 (TRPM8) is subsequently found to be overexpressed in a wide range of cancers and is shown to be implicated in tumorigenesis and tumor progression. Here, we used N-(3-aminopropyl)-2-[(3-methylphenyl) methoxy] -N-(2-thienylmethyl) benzamide hydrochloride (AMTB), a specific TRPM8 antagonist, to explore its antitumoral effect on osteosarcoma. We find that AMTB suppresses osteosarcoma cell proliferation, metastasis and induces cellular apoptosis. Xenograft model in nude mice experiments also define that AMTB can increase the sensitivity of tumor cells to cisplatin, the cytotoxic chemotherapeutic regimens in treating osteosarcoma. Molecularly, AMTB specifically antagonizes TRPM8 which is upregulated in osteosarcoma and its expression level in osteosarcoma tissues is negatively related to patients' prognosis. Finally, RNA sequencing analysis was performed to explore the mechanism underlying the antitumoral effect of AMTB on osteosarcoma cells and the results prove that AMTB suppresses the Transforming Growth Factor β (TGFβ) signaling pathway. Our study provides evidence that TRPM8 could be a potential therapeutic target and AMTB can suppress growth and metastasis of osteosarcoma cells through repressing the TGFβ signaling pathway and increase the sensitivity of tumor cells to cisplatin.

Indexed as

Bone NeoplasmsOsteosarcomaTRPM Cation ChannelsAnimalsCell Line, TumorCell ProliferationCisplatinHumansMaleMembrane ProteinsMiceMice, NudeSignal TransductionTransforming Growth Factor betaCisplatinMembrane ProteinsTransforming Growth Factor betaTRPM8 channel-associated factor 1 protein, humanTRPM8 protein, humanTRPM8 protein, mouseTRPM Cation Channels

Identifiers

PMID35361751
PMCPMC8971393
OpenAlexW4220844228

What OpenQuestion holds

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LicenceCC BY
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.