Evidence map›Paper›PMID 33552281›Full record

ArticleOncology letters2021

Recombinant anthrax lethal toxin inhibits cell motility and invasion in breast cancer cells through the dysregulation of Rho GTPases.

Dana El-Chami, Maria Al Haddad, Ralph Abi-Habib, Mirvat El-Sibai

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

6 citing papers in PubMed, 6 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

4 authors at 1 institution in 1 country.

Dana El-ChamiDepartment of Natural Sciences, School of Arts and Sciences, Lebanese American University, Beirut 1102 2801, Lebanon.
Maria Al HaddadDepartment of Natural Sciences, School of Arts and Sciences, Lebanese American University, Beirut 1102 2801, Lebanon.
Ralph Abi-HabibDepartment of Natural Sciences, School of Arts and Sciences, Lebanese American University, Beirut 1102 2801, Lebanon.
Mirvat El-SibaiDepartment of Natural Sciences, School of Arts and Sciences, Lebanese American University, Beirut 1102 2801, Lebanon.
Lebanese American University · LB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is the leading cause of cancer-associated death among women worldwide. Targeting breast cancer cell metastasis is an important therapeutic approach. The MAPK pathway is a key cell signaling pathway that plays a pivotal role in cellular invasion and migration. Numerous studies have identified the MAPK pathway as a way to target cell survival and motility. The present study treated MBA-MD-231 breast cancer cells with anthrax lethal toxin (LeTx), a potent MAPK inhibitor that selectively cleaves and inactivates all MEKs, as a potential therapeutic method to inhibit breast cancer cell migration. LeTx has been demonstrated to affect breast cancer cell migration. Cells treated with LeTx showed a significant decrease in motility, as observed using wound healing and random 2D motility assays. Additionally, cells treated with LeTx showed an increase in adhesion, which would explain the decrease in migration. Pull-down assays examining the activation status of the members of the Rho family of GTPases revealed an increase in RhoA activation accompanied by a decrease in Cdc42 activation following LeTx treatment. Finally, LeTx mediated a decrease in invasion using a Boyden chamber assay, which could be a result of the decrease in Cdc42 activation. The present study reported the effect of LeTx treatment on the migration, adhesion and invasion of breast cancer cells, demonstrating that this effect was associated with the dysregulation of the Rho GTPases, RhoA and Cdc42.

Indexed as

anthrax lethal toxinbreast cancerinvasionMAPKmigrationRho GTPases

Identifiers

PMID33552281
PMCPMC7798095
OpenAlexW3117583708

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.