Evidence map›Paper›PMID 34006822›Full record

ArticleCell death & disease2021

Sodium/glucose cotransporter 1-dependent metabolic alterations induce tamoxifen resistance in breast cancer by promoting macrophage M2 polarization.

Xingjian Niu, Jianli Ma, Jingtong Li, Yucui Gu, Lei Yin, Yiran Wang, Xiaoping Zhou, Jinlu Wang, Hongfei Ji, Qingyuan Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Immunity and Beyond: Emerging Roles of Monocytes and Macrophages in Cancer.Advances in experimental medicine and biology · 2026
    Review
  6. Review
  7. Review
  8. Review
  9. Tumor-Associated Macrophage in Breast Tumor Microenvironment.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. 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

10 authors at 1 institution in 1 country.

Xingjian Niu *Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, 150081, Heilongjiang, China.
Jianli Ma *Department of Radiation Oncology, Harbin Medical University Cancer Hospital, Harbin, 150081, Heilongjiang, China.
Jingtong LiDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, 150081, Heilongjiang, China.
Yucui GuDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, 150081, Heilongjiang, China.
Lei YinInstitute of Cancer Prevention and Treatment, Harbin Medical University, Harbin, 150081, Heilongjiang, China.
Yiran WangInstitute of Cancer Prevention and Treatment, Harbin Medical University, Harbin, 150081, Heilongjiang, China.
Xiaoping ZhouDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, 150081, Heilongjiang, China.
Jinlu WangDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, 150081, Heilongjiang, China.
Hongfei JiInstitute of Cancer Prevention and Treatment, Harbin Medical University, Harbin, 150081, Heilongjiang, China. jihongfei@hrbmu.edu.cn.
Qingyuan ZhangDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, 150081, Heilongjiang, China. zqyHMU1965@163.com.ORCID 0000-0001-7618-4393
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endocrine therapy is the standard treatment for estrogen receptor (ER)-positive breast cancer, but tumors eventually develop resistance. However, endocrine therapy resistance mechanisms mediated through interactions between breast cancer cells and tumor-associated macrophages (TAMs) are still unclear. Here, we characterized sodium/glucose cotransporter 1 (SGLT1) overexpression drives the highly glycolytic phenotype of tamoxifen-resistant breast cancer cells where enhanced lactic acid secretion promotes M2-like TAM polarization via the hypoxia-inducible factor-1α/signal transducer and activator of transcription-3 pathway. In turn, M2-like TAMs activate breast cancer cells through EGFR/PI3K/Akt signaling, providing feedback to upregulate SGLT1 and promote tamoxifen resistance and accelerate tumor growth in vitro and in vivo. Higher expression of SGLT1 and CD163

Indexed as

AnimalsApoptosisBreast NeoplasmsCell Line, TumorCell ProliferationDrug Resistance, NeoplasmFemaleHumansMacrophagesMiceMice, NudeTamoxifenTransfectionTamoxifen

Identifiers

PMID34006822
PMCPMC8131586
OpenAlexW3162273345

What OpenQuestion holds

Textmetadata
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.