Evidence map›Paper›PMID 28325293›Full record

ArticleMolecular therapy. Nucleic acids2017

A piRNA-like Small RNA Induces Chemoresistance to Cisplatin-Based Therapy by Inhibiting Apoptosis in Lung Squamous Cell Carcinoma.

Yuyan Wang, Tyler Gable, Mark Z Ma, David Clark, Jun Zhao, Yi Zhang, Wei Liu, Li Mao, Yuping Mei

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

Article in Molecular therapy. Nucleic acids, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 51 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

9 authors at 4 institutions in 2 countries.

Yuyan WangDepartment of Oncology and Diagnostic Sciences, University of Maryland School of Dentistry, 650 W. Baltimore St., Baltimore, MD 21201, USA; Department of Thoracic Medical Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Beijing Institute for Cancer Research, Beijing 100142, China.
Tyler GableDepartment of Oncology and Diagnostic Sciences, University of Maryland School of Dentistry, 650 W. Baltimore St., Baltimore, MD 21201, USA.
Mark Z MaDepartment of Oncology and Diagnostic Sciences, University of Maryland School of Dentistry, 650 W. Baltimore St., Baltimore, MD 21201, USA.
David ClarkDepartment of Pathology, Johns Hopkins University, Baltimore, MD 21287, USA.
Jun ZhaoDepartment of Oncology and Diagnostic Sciences, University of Maryland School of Dentistry, 650 W. Baltimore St., Baltimore, MD 21201, USA; Department of Thoracic Medical Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Beijing Institute for Cancer Research, Beijing 100142, China.
Yi ZhangDepartment of Thoracic Surgery, Lung Cancer Center, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.
Wei LiuGuangdong Key Laboratory of Liver Disease Research, Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China.
Li MaoDepartment of Oncology and Diagnostic Sciences, University of Maryland School of Dentistry, 650 W. Baltimore St., Baltimore, MD 21201, USA.
Yuping MeiDepartment of Oncology and Diagnostic Sciences, University of Maryland School of Dentistry, 650 W. Baltimore St., Baltimore, MD 21201, USA. Electronic address: ymei@umaryland.edu.
University of Maryland, Baltimore · USCapital Medical University · CNJohns Hopkins University · USSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer-related death worldwide. Although advanced drugs have benefitted patients, therapeutic success has largely been hampered because of rapid development of resistance. Here we report that PIWI-interacting RNA likes (piR-Ls), a novel type of functional sncRNAs, play key roles in chemoresistance to cisplatin (CDDP)-based chemotherapy in lung squamous cell carcinoma (LSCC). piR-L-138 was upregulated upon CDDP-based chemotherapy both in LSCC cells and in patient-derived xenograft (PDX) LSCC models. Further, targeting upregulated piR-L-138 led to increased apoptosis in CDDP-treated LSCC cells and LSCC xenograft mice treated with CDDP. In addition, piR-L-138 directly interacted with p60-MDM2 and inhibited CDDP-activated apoptosis in p53-mutated LSCC. We identified the upregulated piR-L-138 upon CDDP-based chemotherapy, confirmed the enhanced sensitivity of LSCC to agents by targeting the upregulated piR-L-138 both in vitro and in vivo, and revealed mechanisms underlying piR-L-138 in chemoresistance, bolstering a new emerging clinical modality where novel functional piR-Ls provide potential strategies to overcome chemoresistance for patients with LSCC.

Indexed as

chemoresistancelung cancerpiRNA-likessncRNA

Identifiers

PMID28325293
PMCPMC5363509
OpenAlexW2581582590

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.