Evidence map›Paper›PMID 30847386›Full record

ArticleMolecular therapy oncolytics2019

Nitidine Chloride Inhibits SIN1 Expression in Osteosarcoma Cells.

Hui Xu, Tong Cao, Xiaoqing Zhang, Ying Shi, Qing Zhang, Shuo Chai, Li Yu, Guoxi Jin, Jia Ma, Peter Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy oncolytics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-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

16 citing papers in PubMed, 21 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

11 authors at 2 institutions in 1 country.

Hui XuDepartment of Laboratory Medicine, School of Laboratory Medicine, Bengbu Medical College, Bengbu, Anhui 233030, China.
Tong CaoDepartment of Clinical Laboratory , The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, China.
Xiaoqing ZhangResearch Center of Clinical Laboratory Science, Bengbu Medical College, Bengbu, Anhui 233030, China.
Ying ShiDepartment of Laboratory Medicine, School of Laboratory Medicine, Bengbu Medical College, Bengbu, Anhui 233030, China.
Qing ZhangDepartment of Orthopedics, The Center Hospital of Bengbu, Bengbu, Anhui 233030, China.
Shuo ChaiResearch Center of Clinical Laboratory Science, Bengbu Medical College, Bengbu, Anhui 233030, China.
Li YuDepartment of Laboratory Medicine, School of Laboratory Medicine, Bengbu Medical College, Bengbu, Anhui 233030, China.
Guoxi JinDepartment of Endocrinology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233030, China.
Jia MaDepartment of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, Bengbu, Anhui 233030, China.
Peter WangDepartment of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, Bengbu, Anhui 233030, China.
Yuyun LiDepartment of Laboratory Medicine, School of Laboratory Medicine, Bengbu Medical College, Bengbu, Anhui 233030, China.
Bengbu Medical College · CNFirst Affiliated Hospital of Bengbu Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nitidine chloride (NC) has been demonstrated to exert a tumor-suppressive function in various types of human cancers. However, the detailed mechanism of NC-mediated anti-tumor effects remains elusive. It has been reported that SIN1, a component of mTORC2 (mammalian target of rapamycin complex C2), plays an oncogenic role in a variety of human cancers. Therefore, the inhibition of SIN1 could be useful for the treatment of human cancers. In this study, we explored whether NC triggered an anti-cancer function via the inhibition of SIN1 in osteosarcoma (OS) cells. An MTT assay was performed to measure the effect of NC on the cell growth of osteosarcoma cells, and flow cytometry was used to detect the apoptotic rate of the cells after NC treatment. The expression of SIN1 was detected by western blotting. Wound-healing assay and Transwell chamber invasion assay were conducted to analyze the motility of osteosarcoma cells following NC exposure. We found that exposure to NC led to the inhibition of cell growth, migration, and invasion and the induction of apoptosis. Mechanistically, we found that NC inhibited the expression of SIN1 in osteosarcoma cells. Overexpression of SIN1 abrogated the inhibition of cell growth and motility induced by NC in osteosarcoma cells. Our results indicate that NC exhibits its tumor-suppressive activity via the inhibition of SIN1 in osteosarcoma cells, suggesting that NC could be a potential inhibitor of SIN1 in osteosarcoma.

Indexed as

apoptosisgrowthinvasionnitidine chlorideosteosarcomaSIN1

Identifiers

PMID30847386
PMCPMC6389778
OpenAlexW2912584669

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.