Evidence map›Paper›PMID 34382727›Full record

ArticleCancer science2021

miR-221 confers lapatinib resistance by negatively regulating p27

Thanh Kieu Huynh, Chih-Hao Huang, Jhen-Yu Chen, Jin-Han Yao, Yi-Shiang Yang, Ya-Ling Wei, Hsiao-Fan Chen, Chia-Hung Chen, Chih-Yen Tu, Yuan-Man Hsu and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2021. 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
1.2field-weighted citation impact, top 18% 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, 18 citations in OpenAlex.

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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

12 authors at 3 institutions in 1 country.

Thanh Kieu HuynhGraduate Institute of Biomedical Sciences, Drug Development Center, China Medical University, Taichung, Taiwan.
Chih-Hao HuangGraduate Institute of Biomedical Sciences, Drug Development Center, China Medical University, Taichung, Taiwan.
Jhen-Yu ChenGraduate Institute of Biomedical Sciences, Drug Development Center, China Medical University, Taichung, Taiwan.
Jin-Han YaoSchool of Medicine, China Medical University, Taichung, Taiwan.
Yi-Shiang YangCenter for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan.
Ya-Ling WeiCenter for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan.
Hsiao-Fan ChenCenter for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan.
Chia-Hung ChenSchool of Medicine, China Medical University, Taichung, Taiwan.
Chih-Yen TuSchool of Medicine, China Medical University, Taichung, Taiwan.
Yuan-Man HsuDepartment of Biological Science and Technology, China Medical University, Taichung, Taiwan.
Liang-Chih LiuDivision of Breast Surgery, China Medical University Hospital, Taichung, Taiwan.
Wei-Chien HuangGraduate Institute of Biomedical Sciences, Drug Development Center, China Medical University, Taichung, Taiwan.ORCID https://orcid.org/0000-0001-6467-8716
China Medical University · TWAsia University · TWTunghai University · TW

Funding

China Medical University Hospital DMR-109-021China Medical University Hospital DMR 109-022China Medical University, Taiwan CMU106-ASIA-18China Medical University, Taiwan CMU107-TU-06Ministry of Science Technology, Taiwan MOST 109-2320-B-039-014: MOST 110-2314-B-039-048
6 · The paper itself

Abstract

Development of acquired resistance to lapatinib, a dual epidermal growth factor receptor (EGFR)/human epidermal growth factor receptor 2 (HER2) tyrosine kinase inhibitor, severely limits the duration of clinical response in advanced HER2-driven breast cancer patients. Although the compensatory activation of the PI3K/Akt survival signal has been proposed to cause acquired lapatinib resistance, comprehensive molecular mechanisms remain required to develop more efficient strategies to circumvent this therapeutic difficulty. In this study, we found that suppression of HER2 by lapatinib still led to Akt inactivation and elevation of FOX3a protein levels, but failed to induce the expression of their downstream pro-apoptotic effector p27

Indexed as

AnimalsAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCyclin-Dependent Kinase Inhibitor p27DasatinibDown-RegulationDrug Resistance, NeoplasmErb-b2 Receptor Tyrosine KinasesFemaleForkhead Box Protein O3Hepatocyte Nuclear Factor 3-gammaHumansLapatinibMiceMice, Inbred BALB CAntineoplastic AgentsCDKN1B protein, humanCyclin-Dependent Kinase Inhibitor p27DasatinibERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesForkhead Box Protein O3FOXA3 protein, humanFOXO3 protein, humanHepatocyte Nuclear Factor 3-gammaLapatinibMicroRNAsMIR221, humanNF-kappa B p50 SubunitNFKB1 protein, humanPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktsrc-Family Kinaseslapatinib resistancemiR-221NF-κBp27kip1Src inhibition

Identifiers

PMID34382727
PMCPMC8486195
OpenAlexW3188414630

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.