Evidence map›Paper›PMID 39766038›Full record

ArticleCancers2024

CXCR1 Expression in MDA-PCa-2b Cell Upregulates ITM2A to Inhibit Tumor Growth.

Timothy O Adekoya, Nikia Smith, Parag Kothari, Monique A Dacanay, Yahui Li, Ricardo M Richardson

Abstract read
In one paragraph

Article in Cancers, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. 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

6 authors.

Timothy O AdekoyaCancer Research Program, Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, NC 27707, USA.ORCID 0000-0001-9877-0676
Nikia SmithCancer Research Program, Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, NC 27707, USA.ORCID 0009-0007-6105-9128
Parag KothariCancer Research Program, Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, NC 27707, USA.
Monique A DacanayCancer Research Program, Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, NC 27707, USA.
Yahui LiCancer Research Program, Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, NC 27707, USA.
Ricardo M RichardsonCancer Research Program, Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, NC 27707, USA.ORCID 0000-0003-1768-8932

Funding

Understanding Perceptions of HIV Risk, PrEP, and PrEP use among African American Women Attending an HBCUU54MD012392 · NIMHD · NORTH CAROLINA CENTRAL UNIVERSITY · PI Cherise Baldwin Harrington · 2017 to 2026
$38.1M
Targeting the MEKK2-ERK5 Signaling Node in Triple Negative Breast CancerU54CA156735 · NCI · NORTH CAROLINA CENTRAL UNIVERSITY · PI RICHARDSON, MICHELER RICARDO · 2010 to 2021
$13.0M
Regulation of Chemokine Mediated Leukocyte FunctionsR01AI038910 · NIAID · NORTH CAROLINA CENTRAL UNIVERSITY · PI RICHARDSON, MICHELER RICARDO · 2002 to 2011
$2.3M
REGULATION OF HUMAN INTERLEUKIN-8 RECEPTORSR29AI038910 · NIAID · DUKE UNIVERSITY · PI RICHARDSON, MICHELER RICARDO · 1996 to 2000
$107k
NCI NIH HHS U54 CA156735NIAID NIH HHS R01 AI038910NIAID NIH HHS R29 AI038910NIH HHS AI38910, CA156735, and MD012392NIMHD NIH HHS U54 MD012392
6 · The paper itself

Abstract

backgroundChemokines, along with their receptors, exert critical roles in tumor development and progression. In prostate cancer (PCa), interleukin-8 (IL-8/CXCL8) was shown to enhance angiogenesis, proliferation, and metastasis. CXCL8 activates two receptors, CXCR1 and CXCR2. While CXCR2 expression was shown to promote PCa growth and metastasis, the role of CXCR1 remains unclear.

methodsIn this study, we stably expressed CXCR1 and, as control, CXCR2 in the androgen-dependent PCa cell line MDA-PCa-2b to evaluate the effect of CXCR1 in tumor development.

resultsMDA-PCa-2b-CXCR1 cells showed decreased cell migration, protein kinase-B (AKT) activation, prostate-specific antigen (PSA) expression, cell proliferation, and tumor development in nude mice, relative to MDA-PCa-2b-Vec and MDA-PCa-2b-CXCR2 cells. MDA-PCa-2b-CXCR1 cells also displayed a significant transition to mesenchymal phenotypes as characterized by decreased E-cadherin expression and a corresponding increased level of N-cadherin and vimentin expression. RNA-seq and Western blot analysis revealed a significant increase in the tumor suppressor integral membrane protein 2A (ITM2A) expression in MDA-PCa-2b-CXCR1 compared to control cells. In prostate adenocarcinoma tissue, ITM2A expression was also shown to be downregulated relative to a normal prostate. Interestingly, the overexpression of ITM2A in MDA-PCa-2b cells (MDA-PCa-2b-ITM2A-GFP) inhibited tumor growth similar to that of MDA-PCa-2b-CXCR1.

conclusionsTaken together, the data suggest that CXCR1 expression in MDA-PCa-2b cells may upregulate ITM2A to abrogate tumor development.

Indexed as

androgen receptorCXCR1CXCR2interleukin-8 receptorsITM2Aprostate cancerprostate-specific antigen

Identifiers

PMID39766038
PMCPMC11674668

What Socratic 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 Socratic graph.