Evidence map›Paper›PMID 31281438›Full record

ArticleExperimental and therapeutic medicine2019

Knockdown of lncRNA-HOTAIR downregulates the drug-resistance of breast cancer cells to doxorubicin via the PI3K/AKT/mTOR signaling pathway.

Zhixiang Li, Jun Qian, Jing Li, Chao Zhu

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

Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.

  1. Pooled it
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  13. Non-Coding RNAs in Breast Cancer: Diagnostic and Therapeutic Implications.International journal of molecular sciences · 2024
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  15. Cell Death: Mechanisms and Potential Targets in Breast Cancer Therapy.International journal of molecular sciences · 2024
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7 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Zhixiang LiDepartment of Tumor Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233000, P.R. China.
Jun QianDepartment of Tumor Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233000, P.R. China.
Jing LiDepartment of Tumor Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233000, P.R. China.
Chao ZhuDepartment of Tumor Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233000, P.R. China.
First Affiliated Hospital of Bengbu Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The resistance to chemotherapeutic drugs is a critical feature of breast cancer recurrence and metastasis. Long non-coding RNAs (LncRNAs) serve key roles in tumor drug resistance. LncRNA-HOX transcript antisense RNA (HOTAIR) has been reported to be overexpressed in certain types of cancer and may be closely associated with tumor resistance. The current study aimed to investigate the role of lncRNA-HOTAIR in the regulation of breast cancer resistance to doxorubicin (DOX). A breast cancer cell line (MCF-7) and DOX-resistant breast cancer cell line (DOXR-MCF-7) were utilized in the current study. DOXR-MCF-7 cells were transfected with lncRNA-HOTAIR small interfering RNA (siRNA) and control siRNA. Subsequently, MTT and colony formation assays were performed to assess cell proliferation. Cell apoptosis was also evaluated via flow cytometry. In addition, western blotting and reverse transcription-quantitative polymerase chain reaction were performed to detect the expression of caspase-3, B-cell lymphoma 2, Bcl-2-associated X protein, phosphoinositide 3-kinase (PI3K), protein kinase B (AKT) and mechanistic target of rapamycin (mTOR), and the phosphorylation of PI3K, AKT, and mTOR. The data indicated that lncRNA-HOTAIR silencing decreased cell proliferation and increased apoptosis in MCF-7 and DOXR MCF-7 cells. Furthermore, lncRNA-HOTAIR silencing significantly decreased the phosphorylation of PI3K, AKT and mTOR, indicating that the knockdown of lncRNA-HOTAIR effectively attenuates the resistance of breast cancer cells to DOX by inhibiting the PI3K/AKT/mTOR pathway. In summary, the present study indicated that the knockdown of lncRNA-HOTAIR weakened the resistance of breast cancer cells to DOX via PI3K/AKT/mTOR signaling, suggesting that lncRNA-HOTAIR may be a novel intervention target to reverse DOX-resistance in breast cancer.

Indexed as

breast cancerdoxorubicin resistanceHOX transcript antisense RNAlong non-coding RNAphosphoinositide 3-kinase

Identifiers

PMID31281438
PMCPMC6580102
OpenAlexW2947130426

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.