Evidence map›Paper›PMID 31407170›Full record

ArticleMedical oncology (Northwood, London, England)2019

EMT-related protein expression in polyploid giant cancer cells and their daughter cells with different passages after triptolide treatment.

Xinlu Wang, Minying Zheng, Fei Fei, Chunyuan Li, Jiaxing Du, Kai Liu, Yuwei Li, Shiwu Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.1field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 52 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

8 authors at 3 institutions in 1 country.

Xinlu WangDepartment of Pathology, Tianjin Union Medical Center, Tianjin, 300121, People's Republic of China.
Minying ZhengDepartment of Pathology, Tianjin Union Medical Center, Tianjin, 300121, People's Republic of China.
Fei FeiDepartment of Pathology, Tianjin Union Medical Center, Tianjin, 300121, People's Republic of China.
Chunyuan LiDepartment of Pathology, Tianjin Union Medical Center, Tianjin, 300121, People's Republic of China.
Jiaxing DuDepartment of Pathology, Tianjin Union Medical Center, Tianjin, 300121, People's Republic of China.
Kai LiuDepartment of Pathology, Tianjin Union Medical Center, Tianjin, 300121, People's Republic of China.
Yuwei LiDepartments of Colorectal Surgery, Tianjin Union Medical Center, Tianjin, 300121, People's Republic of China.
Shiwu ZhangDepartment of Pathology, Tianjin Union Medical Center, Tianjin, 300121, People's Republic of China. zhangshiwu666@aliyun.com.ORCID http://orcid.org/0000-0002-5052-2283
Tianjin People's Hospital · CNTianjin University of Traditional Chinese Medicine · CNUnion Hospital · CN

Funding

National Natural Science Foundation of China 81672426
6 · The paper itself

Abstract

Our previous work has demonstrated that paclitaxel can induce the formation of polyploid giant cancer cells (PGCCs) and inhibit tumor growth by reprogramming ovarian cancer epithelial cells to a benign fibroblastic state via epithelial-mesenchymal transition. Here, triptolide (TPL) was used to treat the breast and ovarian cancer lines. The morphologic characteristics and EMT-related protein expression were studied in different generation of cancer cells after TPL treatment. When BT-549 and HEY cells reached 80-90% confluence, TPL was added to BT-549 for 48 h and HEY for 9 h at a concentration of 40 ng/ml. Scattered PGCCs survived from TPL treatment and generated daughter cells, and then were cultured in medium without TPL for at least ten generation. Western blot analysis and immunocytochemical staining were performed to detect the expression levels and subcellular location of EMT-related proteins in control cells and different generation of TPL-induced PGCCs with daughter cells. Furthermore, wound-healing, transwell, cell counting kit-8, and MTT assay were used to compare the alternation of migration, invasion, and proliferation among control cells and different generation of TPL-induced PGCCs with daughter cells. Scattered PGCCs survived from the treatment of TPL and produced small-sized daughter cells 20-30 days after treatment. Compared to the control cells, the first generation of TPL-induced PGCCs with their daughter cells differentially expressed EMT-related proteins including fibronectin, E-cadherin, vimentin, and Twist, and had lower migration, invasion, and proliferation abilities. The abilities of migration, invasion, and proliferation of TPL-induced PGCCs with their daughter cells gradually enhanced as the passages increasing, and markedly exceeded the control cells in the tenth generation. TPL-induced PGCCs with their daughter cells gradually obtain the abilities of invasion and metastasis in vitro as the number of passage increasing, which can be used to mimick the cancer cells subjected to anti-cancer drugs in vivo and may provide some new insights to explore the mechanism of cancer invasion, metastasis and relapse after chemotherapy.

Indexed as

Antineoplastic Agents, AlkylatingBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationDiterpenesEpithelial-Mesenchymal TransitionEpoxy CompoundsFemaleGene Expression Regulation, NeoplasticGiant CellsHumansNeoplasm InvasivenessOvarian NeoplasmsPhenanthrenesPolyploidyAntineoplastic Agents, AlkylatingDiterpenesEpoxy CompoundsPhenanthrenestriptolideEpithelial–mesenchymal transitionPolyploid giant cancer cellsTriptolide

Identifiers

PMID31407170
OpenAlexW2969133078

What OpenQuestion holds

Textmetadata
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.