ArticleBiomedical journal2018
Commentary: Lico A causes ER stress and apoptosis via up-regulating miR-144-3p in human lung cancer cell line H292.
Article in Biomedical journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Xiao-ai-ping injection adjunct with platinum-based chemotherapy for advanced non-small-cell lung cancer: a systematic review and meta-analysis.BMC complementary medicine and therapies · 2020Pooled it
- Polyphenols as Lung Cancer Chemopreventive Agents by Targeting microRNAs.Molecules (Basel, Switzerland) · 2022Review
- Perspectives and controversies regarding the use of natural products for the treatment of lung cancer.Cancer medicine · 2021Review
- Investigating aberrantly expressed microRNAs in peripheral blood mononuclear cells from patients with treatment‑resistant schizophrenia using miRNA sequencing and integrated bioinformatics.Molecular medicine reports · 2020Article
- LncRNA LINC01503 aggravates the progression of cervical cancer through sponging miR-342-3p to mediate FXYD3 expression.Bioscience reports · 2020Article
- Basal-bolus or premixed? Shedding light on optimal insulin regime for type 1 diabetes.Biomedical journal · 2018Article
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3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Natural compound licochalcone A (lico A), a main constituent of flavonoids, has been proved to induce ER stress and apoptosis in cancer cells. However, the underlying anti-tumor mechanism of lico A remains to be clarified in detail. A recently-published report from the journal Frontiers in Pharmacology evaluated the miRNA-based mechanism for lico A on its anti-cancer effect. They found that lico A significantly promoted the tumor-suppressor miR-144-3p expression, so as to up-regulate ER stress-response protein CHOP (CCAAT/-enhancer-binding protein homologous protein) by down-regulating nuclear factor E2-related factor 2 (Nrf2), finally inducing apoptotic cell death in lung cancer. Their findings pave the path toward a more understanding of miRNA-based drugs for cancer treatment in the future.
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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.