Evidence map›Paper›PMID 35501367›Full record

ArticleCommunications biology2022

Polarity protein SCRIB interacts with SLC3A2 to regulate proliferation and tamoxifen resistance in ER+ breast cancer.

Yasuhiro Saito, Shiori Matsuda, Naomi Ohnishi, Keiko Endo, Sanae Ashitani, Maki Ohishi, Ayano Ueno, Masaru Tomita, Koji Ueda, Tomoyoshi Soga and 1 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  4. Targeting estrogen-regulated system xCell death & disease · 2025
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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

11 authors at 3 institutions in 2 countries.

Yasuhiro SaitoInstitute for Advanced Biosciences, Keio University, 246-2 Mizukami, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan. ysaito@ttck.keio.ac.jp.ORCID 0000-0001-7625-5702
Shiori MatsudaInstitute for Advanced Biosciences, Keio University, 246-2 Mizukami, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan.
Naomi OhnishiCancer Proteomics Group, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto, Tokyo, Japan.
Keiko EndoInstitute for Advanced Biosciences, Keio University, 246-2 Mizukami, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan.
Sanae AshitaniInstitute for Advanced Biosciences, Keio University, 246-2 Mizukami, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan.
Maki OhishiInstitute for Advanced Biosciences, Keio University, 246-2 Mizukami, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan.
Ayano UenoInstitute for Advanced Biosciences, Keio University, 246-2 Mizukami, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan.
Masaru TomitaInstitute for Advanced Biosciences, Keio University, 246-2 Mizukami, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan.
Koji UedaCancer Proteomics Group, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto, Tokyo, Japan.ORCID 0000-0001-9066-4959
Tomoyoshi SogaInstitute for Advanced Biosciences, Keio University, 246-2 Mizukami, Kakuganji, Tsuruoka, Yamagata, 997-0052, Japan. soga@sfc.keio.ac.jp.ORCID 0000-0001-9502-2509
Senthil K MuthuswamyDepartment of Medicine and Pathology, Cancer Research Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, 3 Blackfan Circle, Boston, MA, 02215, United States. smuthusw@bidmc.harvard.edu.ORCID 0000-0001-6564-9634
Keio University · JPJapanese Foundation For Cancer Research · JPBeth Israel Deaconess Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Estrogen receptor (ER) positive breast cancer represents 75% of all breast cancers in women. Although patients with ER+ cancers receive endocrine therapies, more than 30% develop resistance and succumb to the disease, highlighting the need to understand endocrine resistance. Here we show an unexpected role for the cell polarity protein SCRIB as a tumor-promoter and a regulator of endocrine resistance in ER-positive breast cancer cells. SCRIB expression is induced by estrogen signaling in a MYC-dependent manner. SCRIB interacts with SLC3A2, a heteromeric component of leucine amino acid transporter SLC7A5. SLC3A2 binds to the N-terminus of SCRIB to facilitate the formation of SCRIB/SLC3A2/LLGL2/SLC7A5 quaternary complex required for membrane localization of the amino acid transporter complex. Both SCRIB and SLC3A2 are required for cell proliferation and tamoxifen resistance in ER+ cells identifying a new role for the SCRIB/SLC3A2 complex in ER+ breast cancer.

Indexed as

Breast NeoplasmsDrug Resistance, NeoplasmFusion Regulatory Protein 1, Heavy ChainMembrane ProteinsTamoxifenTumor Suppressor ProteinsCell ProliferationCytoskeletal ProteinsEstrogensFemaleHumansLarge Neutral Amino Acid-Transporter 1Receptors, EstrogenCytoskeletal ProteinsEstrogensFusion Regulatory Protein 1, Heavy ChainLarge Neutral Amino Acid-Transporter 1llgl2 protein, humanMembrane ProteinsReceptors, EstrogenSCRIB protein, humanSLC3A2 protein, humanSLC7A5 protein, humanTamoxifenTumor Suppressor Proteins

Identifiers

PMID35501367
PMCPMC9061724
OpenAlexW4225278877

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.