ArticleThe Kaohsiung journal of medical sciences2022
miR-96-5p regulates cervical cancer cell resistance to cisplatin by inhibiting lncRNA TRIM52-AS1 and promoting IGF2BP2.
Article in The Kaohsiung journal of medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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.
Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Therapy resistance-related ncRNAs in cervical cancer: biomarkers and therapeutic targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
- Mechanism of N6-methyladenosine (m6A)-mediated upregulation of LINC00958 in the growth of cervical cancer.Frontiers in oncology · 2026Article
- The role of long non-coding RNAs in therapy resistance of cervical cancer and therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Long Noncoding RNA TOB1-AS1 Represses Cervical Cancer Cell Proliferation, Invasion, and Migration via the MicroRNA-27a-3p/Thioredoxin-Interacting Protein Molecular Axis.The Kaohsiung journal of medical sciences · 2025Article
- IGF2BP2: an mCellular & molecular biology letters · 2025Review
- Multifaceted roles of insulin‑like growth factor 2 mRNA binding protein 2 in human cancer (Review).Molecular medicine reports · 2025Review
- Knockdown of IGF2BP2 overcomes cisplatin-resistance in lung cancer through downregulating Spon2 gene.Hereditas · 2024Article
- The Emerging Role of IGF2BP2 in Cancer Therapy Resistance: From Molecular Mechanism to Future Potential.International journal of molecular sciences · 2024Review
- Role of microRNA-4739 in enhancing cisplatin chemosensitivity by negative regulation of RHBDD2 in human cervical cancer cells.Cellular & molecular biology letters · 2024Article
- Expression patterns of mTurkish journal of biology = Turk biyoloji dergisi · 2024Article
- RNA binding proteins in cancer chemotherapeutic drug resistance.Frontiers in cell and developmental biology · 2024Review
- miR-96-5p regulates cervical cancer cell resistance to cisplatin by inhibiting lncRNA TRIM52-AS1 and promoting IGF2BP2.The Kaohsiung journal of medical sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA (miRNA) and long noncoding RNA (lncRNA) are both regulators of cancer progression. This study sought to discuss the functional mechanism of miR-96-5p/lncRNA TRIM52 antisense RNA 1 (head-to-head; TRIM52-AS1) in cervical cancer (CC) cell resistance to cisplatin (DDP). DDP-resistant CC cell line was established using increasing concentrations of DDP, followed by transfection with miR-96-5p inhibitor, or si-TRIM52-AS1, or insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) overexpression vector. Expression levels of miR-96-5p, TRIM52-AS1, and IGF2BP2 were determined. Changes in IC50 value to DDP, cell proliferation, and apoptosis rate were evaluated by cell-counting kit-8 assay, colony formation, and flow cytometry. The bindings of miR-96-5p to IGF2BP2 and TRIM52-AS1 to IGF2BP2 were verified by dual-luciferase or RNA pull-down assays. These experiments revealed an up-expression of miR-96-5p and IGF2BP2 while an under-expression of TRIM52-AS1 in CC cells. After DDP treatment, miR-96-5p inhibition increased apoptosis and decreased proliferation and DDP resistance. miR-96-5p bound to TRIM52-AS1 and downregulated TRIM52-AS1 expression, and TRIM52-AS1 bound to IGF2BP2 to inhibit IGF2BP2 expression. TRIM52-AS1 inhibition or IGF2BP2 overexpression neutralized the inhibition of silencing miR-96-5p on CC cell resistance to DDP. Overall, miR-96-5p improved CC cell resistance to DDP by inhibiting TRIM52-AS1 and promoting IGF2BP2.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.