Evidence map›Paper›PMID 38642607›Full record

ArticleCancer letters2024

Deciphering a GPCR-lncrna-miRNA nexus: Identification of an aberrant therapeutic target in ovarian cancer.

Ji Hee Ha, Rangasudhagar Radhakrishnan, Revathy Nadhan, Rohini Gomathinayagam, Muralidharan Jayaraman, Mingda Yan, Srishti Kashyap, Kar-Ming Fung, Chao Xu, Resham Bhattacharya and 4 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

12 citing papers in PubMed, 11 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

14 authors at 4 institutions in 4 countries.

Ji Hee HaStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA; Department of Cell Biology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Rangasudhagar RadhakrishnanStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Revathy NadhanStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Rohini GomathinayagamStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Muralidharan JayaramanStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA; Department of Cell Biology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Mingda YanStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Srishti KashyapStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Kar-Ming FungStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA; Department of Pathology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Chao XuDepartment of Biostatistics and Epidemiology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Resham BhattacharyaStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA; Department of Obstetrics and Gynecology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Priyabrata MukherjeeStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA; Department of Pathology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA.
Ciro IsidoroDepartment of Health Sciences, Università del Piemonte Orientale, Novara, Italy.
Yong Sang SongSeoul National University, College of Medicine, Seoul, 151-921, South Korea.
Danny N DhanasekaranStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA; Department of Cell Biology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA. Electronic address: danny-dhanasekaran@ouhsc.edu.
OU Health Stephenson Cancer CenterSeoul National University · KRUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITUniversity of Oklahoma Health Sciences Center · US

Funding

Tissue Pathology Shared ResourceP30CA225520 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ROBERT S. MANNEL · 2018 to 2026
$27.1M
TUMOR RESISTANCE MECHANISMS TO ANTI-VEGF THERAPY IN PROSTATE CANCER (Sukyung Woo)P20GM103639 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI DHANASEKARAN, DANNY N. · 2012 to 2022
$21.3M
NCI NIH HHS P30 CA225520NIGMS NIH HHS P20 GM103639
6 · The paper itself

Abstract

Ovarian cancer ranks as a leading cause of mortality among gynecological malignancies, primarily due to the lack of early diagnostic tools, effective targeted therapy, and clear understanding of disease etiology. Previous studies have identified the pivotal role of Lysophosphatidic acid (LPA)-signaling in ovarian cancer pathobiology. Our earlier transcriptomic analysis identified Urothelial Carcinoma Associated-1 (UCA1) as an LPA-stimulated long non-coding RNA (lncRNA). In this study, we elucidate the tripartite interaction between LPA-signaling, UCA1, and let-7 miRNAs in ovarian cancer progression. Results show that the elevated expression of UCA1 enhances cell proliferation, invasive migration, and therapy resistance in high-grade serous ovarian carcinoma cells, whereas silencing UCA1 reverses these oncogenic phenotypes. UCA1 expression inversely correlates with survival outcomes and therapy response in ovarian cancer clinical samples, underscoring its prognostic significance. Mechanistically, UCA1 sequesters let-7 miRNAs, effectively neutralizing their tumor-suppressive functions involving key oncogenes such as Ras and c-Myc. More significantly, intratumoral delivery of UCA1-specific siRNAs inhibits the growth of cisplatin-refractory ovarian cancer xenografts, demonstrating the therapeutic potential of targeting LPAR-UCA1-let-7 axis in ovarian cancer. Thus, our results identify LPAR-UCA1-let-7 axis as a novel avenue for targeted treatment strategies.

Indexed as

Cell MovementCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticMicroRNAsOvarian NeoplasmsRNA, Long NoncodingAnimalsCell Line, TumorCisplatinFemaleHumansLysophospholipidsMiceMice, NudeReceptors, Lysophosphatidic AcidCisplatinLysophospholipidsMicroRNAsReceptors, Lysophosphatidic AcidRNA, Long NoncodingGPCRHigh grade serous ovarian carcinomaLet-7 miRNAslncRNAOncogenic pathwaysOvarian cancerTherapy resistanceUCA1

Identifiers

PMID38642607
PMCPMC12927523
OpenAlexW4394936136

What OpenQuestion holds

Textmetadata
LicenceTDM
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.