Evidence map›Paper›PMID 38416196›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2024

Exploring the therapeutic potential of SGLT2 inhibitors in cancer treatment: integrating in silico and in vitro investigations.

Prasanna Mohite, Deepak K Lokwani, Nikhil S Sakle

Abstract read
PubMed Publisher
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Investigating Vitamin DMolecular diversity · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Research Progress of SGLT2 Inhibitors in Cancer Treatment.Drug design, development and therapy · 2025
    Review
  9. Article
  10. 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

3 authors at 1 institution in 1 country.

Prasanna MohiteDr. Rafiq Zakaria Campus, Y. B. Chavan College of Pharmacy, Aurangabad, 431001, Maharashtra, India.
Deepak K LokwaniDepartment of Pharmaceutical Chemistry, Rajarshi Shahu College of Pharmacy, Buldana, Maharashtra, India.ORCID http://orcid.org/0000-0003-2858-678X
Nikhil S SakleDr. Rafiq Zakaria Campus, Y. B. Chavan College of Pharmacy, Aurangabad, 431001, Maharashtra, India. nikhilsakle@gmail.com.ORCID http://orcid.org/0000-0003-2614-1920
Government Medical College · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study aimed to investigate the anti-cancer mechanism of canagliflozin (CANA) and dapagliflozin (DAPA), sodium-glucose co-transporter-2 (SGLT2) inhibitors, using in silico and in vitro approaches. Network pharmacology was employed to predict the targets of the inhibitors and GO gene enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotation conducted to explore the interacting pathways. Molecular docking and molecular dynamic (MD) simulation studies were performed to confirm the important targets and assess conformational stability. In vitro cytotoxicity assays, MIA-PaCa-2 and DU-145 cell lines CANA and DAPA was performed. Protein-protein interaction (PPI) network analysis indicated that CANA and DAPA exert anticancer effects through MAPK, mTOR, EGFR-KRAS-BRAF, FGFR, and PI3KA pathways. KEGG analysis revealed that these inhibitors could be used in the treatment of various cancers, including breast, prostate, pancreatic, chronic myeloid leukemia, thyroid, small cell lung, gastric, and bladder cancer. Docking results showed highest affinity for MAPK1 for CANA (- 9.60 kcal/mol) and DAPA (- 9.58 kcal/mol). MD simulation results showed that RMSD values for the MAPK1-compound exhibit remarkable stability over a timeframe of 100 ns. In cytotoxicity assays using MIA-PaCa-2 and DU-145 cell lines, CANA demonstrated a potential antiproliferative effect on the pancreatic cell line MIA-PaCa-2 after 48 h of treatment at a concentration of 100 µg/ml. Furthermore, CANA arrested the cell cycle in the sub-G1 phase and induced late apoptosis and necrosis in MIA-PaCa-2 cell line. Based on these findings, CANA shows promise as a potential novel treatment strategy for pancreatic cancer.

Indexed as

Antineoplastic AgentsBenzhydryl CompoundsCanagliflozinMolecular Docking SimulationNeoplasmsSodium-Glucose Transporter 2 InhibitorsApoptosisCell Line, TumorCell ProliferationCell SurvivalComputer SimulationGlucosidesHumansMolecular Dynamics SimulationProtein Interaction MapsSodium-Glucose Transporter 2Antineoplastic AgentsBenzhydryl CompoundsCanagliflozindapagliflozinGlucosidesSLC5A2 protein, humanSodium-Glucose Transporter 2Sodium-Glucose Transporter 2 InhibitorsCancerMolecular dockingMolecular dynamics simulationNetwork pharmacologySGLT-2 inhibitors

Identifiers

PMID38416196
OpenAlexW4392234072

What OpenQuestion holds

Textmetadata
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.