Evidence map›Paper›PMID 31529191›Full record

ArticleJournal of cancer research and clinical oncology2019

CD44 splice variant (CD44v3) promotes progression of urothelial carcinoma of bladder through Akt/ERK/STAT3 pathways: novel therapeutic approach.

Vivek Anand, Madhuram Khandelwal, Sandeep Appunni, Nidhi Gupta, Amlesh Seth, Prabhjot Singh, Sandeep Mathur, Alpana Sharma

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

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  5. CD44 variant exons induce chemoresistance by modulating cell death pathways.Frontiers in cell and developmental biology · 2025
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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 1 institution in 1 country.

Vivek AnandDepartment of Biochemistry, All India Institute of Medical Sciences (AIIMS), New Delhi, 110029, India.
Madhuram KhandelwalDepartment of Biochemistry, All India Institute of Medical Sciences (AIIMS), New Delhi, 110029, India.
Sandeep AppunniDepartment of Biochemistry, All India Institute of Medical Sciences (AIIMS), New Delhi, 110029, India.
Nidhi GuptaDepartment of Biochemistry, All India Institute of Medical Sciences (AIIMS), New Delhi, 110029, India.
Amlesh SethDepartment of Urology, All India Institute of Medical Sciences (AIIMS), New Delhi, India.
Prabhjot SinghDepartment of Urology, All India Institute of Medical Sciences (AIIMS), New Delhi, India.
Sandeep MathurDepartment of Pathology, All India Institute of Medical Sciences (AIIMS), New Delhi, India.
Alpana SharmaDepartment of Biochemistry, All India Institute of Medical Sciences (AIIMS), New Delhi, 110029, India. dralpanasharma@gmail.com.ORCID http://orcid.org/0000-0001-7761-5511
All India Institute of Medical Sciences · IN

Funding

Indian Council of Medical Research 5/13/50/10/NCD-III
6 · The paper itself

Abstract

purposeThe incidence of Urothelial carcinoma of bladder (UBC) is gradually increasing by changing lifestyle and environment. The development of a tumor has been noted to be accompanied by modifications in the extracellular matrix (ECM) consisting of CD44, hyaluronic acid (HA) and its family members. The importance of CD44 splice variants and HA family members has been studied in UBC.

methodsThe cohort of study included 50 UBC patients undergoing radical cystectomy and 50 healthy subjects. The molecular expression of CD44 and HA family members was determined. Effect of CD44 variant-specific silencing on downstream signaling in HT1376 cells was investigated. Combinatorial treatment of 4-MU (4-methylumbelliferone) with cisplatin or doxorubicin on chemosensitivity was also explored.

resultsHigher expression of HA, HAS2, and CD44 was observed in Indian UBC patients which also showed the trend with severity of disease. Splice variant assessment of CD44 demonstrated the distinct role of CD44v3 and CD44v6 in bladder cancer progression. shRNA-mediated downregulation of CD44v3 showed an increase effect on cell cycle, apoptosis and multiple downstream signaling cascade including pAkt, pERK and pSTAT3. Furthermore, 4-MU, an HA synthesis inhibitor, observed to complement the effect of Cisplatin or Doxorubicin by enhancing the chemosensitivity of bladder cancer cells.

conclusionsOur findings exhibit involvement of CD44 splice variants and HA family members in UBC and significance of 4-MU in enhancing chemosensitivity suggesting their novel therapeutic importance in disease therapeutics.

Indexed as

Alternative SplicingAdenocarcinomaApoptosisCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansHyaluronan ReceptorsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PrognosisProto-Oncogene Proteins c-aktSTAT3 Transcription FactorTumor Cells, CulturedUrinary Bladder NeoplasmsAKT1 protein, humanCD44 protein, humanHyaluronan ReceptorsMAPK1 protein, humanMAPK3 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene Proteins c-aktSTAT3 protein, humanSTAT3 Transcription Factor4-MethylumbelliferoneBladder cancerCD44CD44 variant 3Hyaluronic acidHyaluronic acid synthase

Identifiers

PMID31529191
PMCPMC11810428
OpenAlexW2973553336

What OpenQuestion holds

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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 OpenQuestion graph.