Evidence map›Paper›PMID 30808417›Full record

ArticleBiological research2019

Derlin1 functions as an oncogene in cervical cancer via AKT/mTOR signaling pathway.

Ling Li, Ming Liu, Zhihu Zhang, Wei Zhang, Naifu Liu, Xiugui Sheng, Ping Wei

Open access · goldAbstract readLetter
In one paragraph

Article in Biological research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
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

7 authors at 5 institutions in 1 country.

Ling LiDepartment of Oncology, People's Hospital of Tengzhou City, Tengzhou, 277599, Shandong, China.
Ming LiuDepartment of Gynecologic Oncology, Shandong Tumor Hospital and Institute, No. 440, Yan Ji Road, Jinan, 250117, Shandong, China.
Zhihu ZhangShandong Academy of Occupational Health and Medicine, Jinan, 250062, Shandong, China.
Wei ZhangDepartment of Obstetrics and Gynecology, Affiliated Hospital of Binzhou Medical College, Binzhou, Shandong, China.
Naifu LiuDepartment of Gynecologic Oncology, Shandong Tumor Hospital and Institute, No. 440, Yan Ji Road, Jinan, 250117, Shandong, China.
Xiugui ShengDepartment of Gynecologic Oncology, Tumor Hospital of Chinese Academy of Medical Sciences, Shenzhen, 518116, China.
Ping WeiDepartment of Gynecologic Oncology, Shandong Tumor Hospital and Institute, No. 440, Yan Ji Road, Jinan, 250117, Shandong, China. zyhwp@163.com.
Shandong Tumor Hospital · CNBinzhou Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNShandong Academy of Chinese Medicine · CNTengzhou Central People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCervical cancer (CC) ranks third in the morbidity and mortality of female cancer around the world. Derlin1 has been found to be overexpressed in several human cancers. However, it is still unclear about its roles in CC. The research aims to explore the relationship between Derlin1 and CC.

methodsWe purchased a human CC tissues microarray, which contained CC tissues and corresponding para-cancerous tissues from 93 patients with primary cervical squamous cell carcinoma. Immunohistochemical staining was used to confirm the expression of Derlin1 in these tissues. And we detected the differential expression of Derlin1 in cervical cancer cell lines and normal cervical epithelial cells (H8). Further, the cervical cancer cell lines SiHa and C33A were used as an in vitro model, which was down-regulated the expression of Derlin1 using siRNA interference technology. The effects of Derlin1 down-regulating in CC cell lines on cell proliferation and migration were detected by CCK8 assay and transwell assay, respectively. The effect of Derlin1 down-regulating on apoptosis was analyzed by flow cytometry, and apoptosis-related proteins were detected using western blotting. In-depth mechanisms were studied using western blotting. In addition, the effects of Derlin1 up-regulating in normal cervical epithelial cells also were exposed.

resultsDerlin1 was significantly elevated in CC tissues (81.7%, 76/93), and the expression of Derlin1 was positively correlated with the tumor size, pathological grade, and lymph node metastasis in CC patients. And Derlin1 was high expressed in cervical cancer cell lines compared to H8 cells. Knockdown of Derlin1 in cervical cancer cell lines inhibited cell proliferation and migration. Moreover, knockdown of Derlin1 induced apoptosis and affected the expression of apoptosis-related proteins, including Bcl-2, Bax, Bim, caspase3 and caspase9. Further experiments showed that AKT/mTOR signal pathway might be involve in this processes that knockdown of Derlin1 inhibited the expression of p-AKT and p-mTOR. Over-expression of Derlin1 in H8 cells promoted cell proliferation and migration via up-regulated the expression of p-AKT and p-mTOR.

conclusionDerlin1 is an oncogene in CC via AKT/mTOR pathway. It might be a potential therapeutic target for CC.

Indexed as

ApoptosisCarcinoma, Squamous CellCell Line, TumorCell ProliferationFemaleHumansImmunohistochemistryMembrane ProteinsProtein Array AnalysisProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesUterine Cervical NeoplasmsDERL1 protein, humanMembrane ProteinsMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAKT/mTORBaxBcl-2Cervical cancerDerlin1

Identifiers

PMID30808417
PMCPMC6391802
OpenAlexW2927353153

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.