ArticleInternational journal of clinical and experimental pathology2018
Knockdown of SALL4 overcomes cisplatin-resistance through AKT/mTOR signaling in lung cancer cells.
Article in International journal of clinical and experimental pathology, 2018. 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
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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.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Embryonic stem cell factors DPPA2/4 amplify active H3K4me3-H2AK119ub chromatin domains in non-small cell lung cancer.Genes & development · 2026Article
- SALL4-targeted therapeutic peptide PEN-FFW suppresses PD-L1 and enhances CD8⁺ T cell cytotoxicity via regulating PI3K/AKT signaling in breast cancer.Immunologic research · 2026Article
- Review
- Silencing AREG Enhances Sensitivity to Irradiation by Suppressing the PI3K/AKT Signaling Pathway in Colorectal Cancer Cells.Biologics : targets & therapy · 2024Article
- Global comparative transcriptomes uncover novel and population-specific gene expression in esophageal squamous cell carcinoma.Infectious agents and cancer · 2023Article
- SALL4 promotes angiogenesis in gastric cancer by regulating VEGF expression and targeting SALL4/VEGF pathway inhibits cancer progression.Cancer cell international · 2023Article
- The new advance of SALL4 in cancer: Function, regulation, and implication.Journal of clinical laboratory analysis · 2023Review
- Role of SALL4 in HER2+ Breast Cancer Progression: Regulating PI3K/AKT Pathway.International journal of molecular sciences · 2022Article
- Review
- SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022Review
- Metformin impairs cisplatin resistance effects in A549 lung cancer cells through mTOR signaling and other metabolic pathways.International journal of oncology · 2021Article
- Knockdown ofAnnals of translational medicine · 2020Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance is an important factor for the poor prognosis of non-small cell lung cancer (NSCLC). Sal-like protein 4 (Sall4) is a stem cell marker, and plays a role in maintaining self-renewal. Previous studies have demonstrated that Sall4 may be a candidate for use as support in the diagnosis of lung cancer, and may also represent a therapeutic target. However, the role of Sall4 on drug resistance of lung cancer cells and the mechanism by which Sall4 regulates the sensitivity of lung cancer cells to cisplatin (DDP) remains unknown. In this study, we aim to investigate whether knockdown of Sall4 by siRNA can enhance the apoptosis induced by cisplatin in lung cancer cells. We here reported that the expression of Sall4 was dramatically upregulated in cisplatin-resistant A549 cells compared with the parental cells. Knockdown of Sall4 by siRNA in cisplatin-resistant A549 cells reduced the IC
Indexed as
Identifiers
31938149PMC6958024W3027409271What Socratic 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 Socratic graph.