Evidence map›Paper›PMID 40849687›Full record

ReviewAsian Pacific journal of cancer prevention : APJCP2025

The Functional Interplay among GAD2, GABRG2, and CACNA1G Genes in Cancers.

Sagung Rai Indrasari, Salma Darmayanti, Adila Zafrullah, Nina Sakina Lessy, Sofia Mubarika Haryana, Ahmad Hamim Sadewa, Risky Oktriani

Abstract readReview
In one paragraph

Review in Asian Pacific journal of cancer prevention : APJCP, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

7 authors.

Sagung Rai IndrasariDepartment of Otorhinolaryngology-Head and Neck Surgery, Faculty of Medicine Public Health and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia.ORCID 0000-0002-4281-8105
Salma DarmayantiMaster's Program in Biomedical Sciences, Faculty of Medicine Public Health and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia.
Adila ZafrullahMaster's Program in Biomedical Sciences, Faculty of Medicine Public Health and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia.
Nina Sakina LessyMaster's Program in Biomedical Sciences, Faculty of Medicine Public Health and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia.
Sofia Mubarika HaryanaCollaboration Research Center for Precision Oncology based Omics (PKR PrOmics), Yogyakarta, Indonesia.ORCID 0000-0001-7205-652X
Ahmad Hamim SadewaDepartment of Biochemistry, Faculty of Medicine Public Health and Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia.
Risky OktrianiCollaboration Research Center for Precision Oncology based Omics (PKR PrOmics), Yogyakarta, Indonesia.ORCID 0000-0001-6809-7871

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The GABAergic system, commonly known as the inhibitory system in the central nervous system, also plays a crucial role in cancer development.

objectiveThis article reviews the complex interactions between the GABAergic system and tumor progression, emphasizing the GAD2, GABRG2, and CACNA1G genes.

methodA comprehensive literature review was conducted to assess current evidence regarding the involvement of GAD2, GABRG2, and CACNA1G genes in promoting cancer development through enhanced tumor growth, cell survival, and increased intracellular calcium levels.

resultWhile GABA generally suppresses neural activity, it can paradoxically promote cell proliferation and survival in cancer cells. The GAD2 gene produces an enzyme that helps create GABA. Higher levels of GAD2 expression have been linked to tumor growth and survival in several types of cancer. The GABRG2 gene encodes a subunit of the GABA-A receptor. When this receptor is activated, it can cause depolarization and activate signaling pathways that promote cancer cell growth. The CACNA1G gene encodes a subunit of a calcium channel that controls calcium ion entry into cells. Higher levels of CACNA1G expression are frequently found in various cancers, contributing to tumor development by increasing intracellular calcium levels.

conclusionThis article examines the role of GAD2, GABRG2, and CACNA1G genes in cancer progression, highlighting their interactions in promoting tumor growth and survival. A deeper understanding of the molecular mechanisms underlying GABA signaling, its receptors, and the associated genes in cancer could lead to the identification of new therapeutic targets and the development of more effective treatments. Further research is essential to elucidate the detailed mechanisms driving cancer development and progression.

Indexed as

Calcium Channels, T-Typegamma-Aminobutyric AcidGlutamate DecarboxylaseNeoplasmsReceptors, GABA-AAnimalsCalciumCalcium SignalingCarcinogenesisCell ProliferationCell SurvivalDisease ProgressionGene Expression Regulation, NeoplasticHumansCACNA1G protein, humanCalciumCalcium Channels, T-TypeGABRG2 protein, humangamma-Aminobutyric AcidGlutamate Decarboxylaseglutamate decarboxylase 2Receptors, GABA-AGABAergic systemgenes interplaymolecular mechanism

Identifiers

PMID40849687
PMCPMC12659877

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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.