Evidence map›Paper›PMID 26993770›Full record

ArticleOncotarget2016

MicroRNA-16 sensitizes breast cancer cells to paclitaxel through suppression of IKBKB expression.

Xueyuan Tang, Long Jin, Peiguo Cao, Ke Cao, Chenghui Huang, Yanwei Luo, Jian Ma, Shourong Shen, Ming Tan, Xiayu Li and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

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  12. A Compressive Review about TaxolMolecules (Basel, Switzerland) · 2020
    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

11 authors at 4 institutions in 3 countries.

Xueyuan TangDepartment of Oncology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Long JinDepartment of Oncology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Peiguo CaoDepartment of Oncology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Ke CaoDepartment of Oncology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Chenghui HuangDepartment of Oncology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Yanwei LuoThe Key Laboratory of Carcinogenesis of The Chinese Ministry of Health and The Key Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China.
Jian MaThe Key Laboratory of Carcinogenesis of The Chinese Ministry of Health and The Key Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China.
Shourong ShenDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Ming TanMitchell Cancer Institute, University of South Alabama, Mobile, Alabama, USA.
Xiayu LiDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Ming ZhouThe Key Laboratory of Carcinogenesis of The Chinese Ministry of Health and The Key Laboratory of Carcinogenesis and Cancer Invasion of The Chinese Ministry of Education, Cancer Research Institute, Central South University, Changsha, Hunan, China.
Central South University · CNThird Xiangya Hospital · CNMinistry of Health · UGUniversity of South Alabama · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paclitaxel (Taxol) is an effective chemotherapeutic agent for treating breast cancer patients. However, chemoresistance is a major obstacle in cancer treatment. Here, we showed that overexpression of miR-16 promoted Taxol-induced cytotoxicity and apoptosis in breast cancer cells. Furthermore, IκB kinase β (IKBKB) was identified as a direct target of miR-16. Up-regulation of IKBKB suppressed Taxol-induced apoptosis and led to an increased resistance to Taxol, and restoring IKBKB expression in miR-16-overexpressing breast cancer cells recovered Taxol resistance. Moreover, miR-16 was highly expressed in Taxol-sensitive breast cancer tissues compared with Taxol-resistant tissues, and there was an inverse correlation between miR-16 expression and IKBKB expression in breast cancer tissues. The expression levels of miR-16 were negatively associated with T stages, whereas the expression of IKBKB was positively correlated with T stages, lymph node metastasis and clinical stages. Taken together, our data demonstrates that miR-16 sensitizes breast cancer cells to Taxol through the suppression of IKBKB expression, and targeting miR-16/IKBKB axis will be a promising strategy for overcoming Taxol resistance in breast cancer.

Indexed as

Antineoplastic Agents, PhytogenicApoptosisBiomarkers, TumorBreast NeoplasmsCarcinoma, Ductal, BreastCarcinoma, LobularCell ProliferationDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansI-kappa B KinaseLymphatic MetastasisMicroRNAsMiddle AgedNeoplasm InvasivenessAntineoplastic Agents, PhytogenicBiomarkers, TumorI-kappa B KinaseIKBKB protein, humanMicroRNAsMIRN16 microRNA, humanPaclitaxelbreast cancerchemosensitivityIKBKBmiR-16Taxol

Identifiers

PMID26993770
PMCPMC5029655
OpenAlexW2325712553

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.