Evidence map›Paper›PMID 32500187›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2021

GLUT1 participates in tamoxifen resistance in breast cancer cells through autophagy regulation.

Mengqi Sun, Shu Zhao, Yuchen Duan, Yumeng Ma, Yicheng Wang, Hongfei Ji, Qingyuan Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2021. 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
2.3field-weighted citation impact, top 11% 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, 68 citations in OpenAlex.

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  9. Breast Cancer Chemoresistance: Insights into the Regulatory Role of lncRNA.International journal of molecular sciences · 2023
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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

7 authors at 3 institutions in 1 country.

Mengqi SunDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, Heilongjiang, 150081, People's Republic of China.
Shu ZhaoDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, Heilongjiang, 150081, People's Republic of China.
Yuchen DuanDepartment of Cardiology, the First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, Heilongjiang, 150001, People's Republic of China.
Yumeng MaDepartment of Ultrasound, the Second Affiliated Hospital of Harbin Medical University, 157 Baojian Road, Harbin, Heilongjiang, 150081, People's Republic of China.
Yicheng WangCollege of Bioinformatics Science and Technology, Harbin Medical University, 157 Baojian Road, Harbin, Heilongjiang, 150081, People's Republic of China.
Hongfei JiHeilongjiang Cancer Research and Prevention Institute, 150 Haping Road, Harbin, Heilongjiang, 150081, People's Republic of China.
Qingyuan ZhangDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, 150 Haping Road, Harbin, Heilongjiang, 150081, People's Republic of China. zhangqingyuan@hrbmu.edu.cn.
Harbin Medical University · CNSecond Affiliated Hospital of Harbin Medical University · CNThird Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tamoxifen is an estrogen modulator widely used in the treatment of patients with ESR/ER-positive breast cancer; however, resistance limits its clinical application. Autophagy alterations have recently been suggested as a new mechanism for tamoxifen resistance. Glucose transporter 1 (GLUT1) has been reported to be associated with the development and metastasis of breast cancer, but the relationship among GLUT1, autophagy, and endocrine resistance remains unclear. Our present study found that GLUT1 expression and autophagy flux were upregulated in the tamoxifen-resistant breast cancer cell line MCF-7/TAMR-1 and that knockdown of GLUT1 promoted sensitization to tamoxifen. Moreover, knockdown of GLUT1 significantly decreased the enhancement of autophagy flux in tamoxifen-resistant cell lines. Furthermore, inhibiting autophagy in tamoxifen-resistant cells resulted in sensitization to tamoxifen. We conclude that GLUT1 contributes to tamoxifen resistance in breast cancer and that tamoxifen-resistant cells become resensitized to tamoxifen after GLUT1 silencing. These findings suggest GLUT1 as a new factor clinically associated with resistance to tamoxifen.

Indexed as

Drug Resistance, NeoplasmAntineoplastic Agents, HormonalAutophagyBreast NeoplasmsCell Line, TumorEstrogen AntagonistsFemaleGlucose Transporter Type 1HumansMiddle AgedRNA, Small InterferingTamoxifenTranscriptomeAntineoplastic Agents, HormonalEstrogen AntagonistsGlucose Transporter Type 1RNA, Small InterferingSLC2A1 protein, humanTamoxifenAutophagyBreast cancerGLUT1Tamoxifen resistance

Identifiers

PMID32500187
OpenAlexW3033132033

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.