Evidence map›Paper›PMID 32158232›Full record

ArticleOncoTargets and therapy2020

Effects of Atypical Protein Kinase C Inhibitor (DNDA) on Lung Cancer Proliferation and Migration by PKC-ι/FAK Ubiquitination Through the Cbl-b Pathway.

Raja Reddy BommaReddy, Rekha Patel, Tracess Smalley, Mildred Acevedo-Duncan

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. 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
0.4field-weighted citation impact, top 40% 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, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Role of RhoC in cancer cell migration.Cancer cell international · 2021
    Review
  5. Protein Kinase C as a Therapeutic Target in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2021
    Review
  6. Review
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.

Raja Reddy BommaReddyDepartment of Chemistry, University of South Florida, Tampa, FL 33620, USA.
Rekha PatelDepartment of Chemistry, University of South Florida, Tampa, FL 33620, USA.
Tracess SmalleyDepartment of Chemistry, University of South Florida, Tampa, FL 33620, USA.
Mildred Acevedo-DuncanDepartment of Chemistry, University of South Florida, Tampa, FL 33620, USA.
University of South Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe options for treating lung cancers are limited, as diagnosis typically occurs during the late stages of the disease. There is a dire need to develop aPKC (atypical Protein Kinase C) inhibitors due to aPKC overexpression and contributions to lung cancer malignancies. In this study, we investigate the role of atypical PKCs (aPKCs) in cell proliferation and migration in lung cancer cell lines and the effect of the novel aPKC inhibitor DNDA (3,4-amino-2,7 napthalene disulfonic acid).

methodsThe normal and lung cancer cells were treated with various concentrations of DNDA. We used a WST assay to determine lung cell viability, then analyzed cell apoptosis through Annexin V/PI staining and flow cytometry. Immunoprecipitation determined the proteins' associations, and Western blot allowed testing of the expression of interest proteins. We also employed the UbiTest to identify the ubiquitination of the FAK. The scratch and transwell assays measured cell migration and invasion of lung cancer cells.

resultsOur data from cell viability and flow cytometry showed a significant reduction in cell proliferation and induction of apoptosis with DNDA treatment in lung cancer cells, as well as no toxic effect on normal BEAS-2B lung cells. Western blot results showed that the phosphorylation of PKC-iota and phosphorylation of FAK decreased in A549 lung cancer cells upon DNDA treatment. Immunoprecipitation (IP) data revealed an association of PKC-ι with FAK and FAK with Casitas B-lineage lymphoma proto-oncogene-b (Cbl-b). UbiTest results suggest that PKC-ι regulates FAK cleavage through its ubiquitination by Cbl-b, thereby inhibiting A549 lung cancer cells' migration. This was evident from scratch, invasion, and migration assays.

conclusionOur study data suggest that DNDA inhibits cell proliferation and induces apoptosis in lung cancer cells. Moreover, DNDA inhibit A549 lung cancer cells' migration by PKC- ι/FAK ubiquitination via Cbl-b.

Indexed as

aPKC inhibitorFAKmigrationNSCLCubiquitination

Identifiers

PMID32158232
PMCPMC7047975
OpenAlexW3007759077

What Socratic holds

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LicenceCC BY-NC
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Registered trials

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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 Socratic graph.