Evidence map›Paper›PMID 30449704›Full record

ArticleStem cell reports2018

Enhancement of Sensitivity to Chemo/Radiation Therapy by Using miR-15b against DCLK1 in Colorectal Cancer.

Dengbo Ji, Tiancheng Zhan, Ming Li, Yunfeng Yao, Jinying Jia, Haizhao Yi, Meng Qiao, Jinhong Xia, Zhiqian Zhang, Huirong Ding and 3 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing 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

41 citing papers in PubMed, 60 citations in OpenAlex.

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  17. Functional assessment of miR‑1291 in colon cancer cells.International journal of oncology · 2022
    Article
  18. The Roles of Non-Coding RNAs in Radiotherapy of Gastrointestinal Carcinoma.Frontiers in cell and developmental biology · 2022
    Review
  19. 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

13 authors at 4 institutions in 1 country.

Dengbo JiKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Department of Gastrointestinal Surgery III, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China.
Tiancheng ZhanKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Department of Gastrointestinal Surgery III, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China.
Ming LiKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Department of Gastrointestinal Surgery III, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China.
Yunfeng YaoKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Department of Gastrointestinal Surgery III, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China.
Jinying JiaKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Department of Gastrointestinal Surgery III, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China.
Haizhao YiKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Department of Gastrointestinal Surgery III, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China.
Meng QiaoKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Department of Gastrointestinal Surgery III, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China.
Jinhong XiaKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Department of Gastrointestinal Surgery III, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China.
Zhiqian ZhangDepartment of Cell Biology, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China.
Huirong DingCentral Laboratory, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China.
Can SongSchool of Life Sciences, Tsinghua University, Beijing 100084, China; Peking-Tsinghua Center for Life Sciences, Beijing 100084, China.
Yong HanDepartment of Pathology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, China.
Jin GuKey Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Department of Gastrointestinal Surgery III, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China; Peking-Tsinghua Center for Life Sciences, Beijing 100084, China; Peking University S.G. Hospital, Beijing 100144, China. Electronic address: zlguj@bjmu.edu.cn.
Peking University Cancer Hospital · CNPeking University · CNCenter for Life Sciences · CNZhejiang Provincial People's Hospital · CN

Funding

1/4 Alcohol Research Consortium in HIV-Administrative Core (ARCH-AC)U24AA020801 · NIAAA · JOHNS HOPKINS UNIVERSITY · PI CHANDER, GEETANJALI, MCCAUL, MARY E · 2011 to 2021
$3.5M
NIAAA NIH HHS U24 AA020801
6 · The paper itself

Abstract

Chemo-/radiotherapy resistance is the main cause accounting for most treatment failure in colorectal cancer (CRC). Tumor-initiating cells (TICs) are the culprit leading to CRC chemo-/radiotherapy resistance. The underlying regulation mechanism of TICs in CRC remains unclear. Here we discovered that miR-15b expression positively correlated with therapeutic outcome in CRC. Expression of miR-15b in pretreatment biopsy tissue samples predicted tumor regression grade (TRG) in rectal cancer patients after receiving neoadjuvant radiotherapy (nRT). Expression of miR-15b in post-nRT tissue samples was associated with therapeutic outcome. DCLK1 was identified as the direct target gene for miR-15b and its suppression was associated with self-renewal and tumorigenic properties of DCLK1+ TICs. We identified B lymphoma Mo-MLV insertion region l homolog (BMI1) as a downstream target regulated by miR-15b/DCLK1 signaling. Thus, miR-15b may serve as a valuable marker for prognosis and therapeutic outcome prediction. DCLK1 could be a potential therapeutic target to overcome chemo-/radioresistance in CRC.

Indexed as

AnimalsBase SequenceCarcinogenesisCell Line, TumorCell Self RenewalChemotherapy, AdjuvantColorectal NeoplasmsDoublecortin-Like KinasesDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMaleMice, Inbred NODMice, SCIDBMI1 protein, humanDCLK1 protein, humanDoublecortin-Like KinasesIntracellular Signaling Peptides and ProteinsMicroRNAsMIRN15 microRNA, humanPolycomb Repressive Complex 1Protein Serine-Threonine Kinaseschemo-/radiotherapycolorectal cancerDCLK1miR-15b

Identifiers

PMID30449704
PMCPMC6294114
OpenAlexW2901728462

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.