ArticleCells2021
YAP-Dependent BiP Induction Is Involved in Nicotine-Mediated Oral Cancer Malignancy.
Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 24 citations in OpenAlex.
- AMPylation: key roles in biological regulation across prokaryotes and eukaryotes.Frontiers in cellular and infection microbiology · 2026Review
- Exploring Molecular Targets of Quercetin for the Treatment of Nicotine-Related Oral Carcinoma: A Network Pharmacology Analysis and In Vitro Study.Food science & nutrition · 2025Article
- The Biological and Prognostic Implications of the Nicotinic Acetylcholine Receptor α3, α5, and α7 Subunits in Oral Squamous Cell Carcinoma.Cancer medicine · 2025Article
- The role of acetylcholine and its receptors in tumor immune regulation: mechanisms and potential therapeutic targets.Molecular cancer · 2025Review
- Predictive Value and Immunological Role of the HSPA5 Gene in Cervical Cancer.Biochemical genetics · 2025Article
- Decoding Oral Carcinogenesis and Tumor Progression in Whole Cigarette Smoke Exposure: A Systematic Review.Cureus · 2024Review
- Nicotine-induced activation of cholinergic receptor nicotinic alpha 5 subunit mediates the malignant behaviours of laryngeal squamous epithelial cells by interacting with RABL6.Cell death discovery · 2024Article
- Targeting Alpha7 Nicotinic Acetylcholine Receptors in Lung Cancer: Insights, Challenges, and Therapeutic Strategies.ACS pharmacology & translational science · 2024Review
- MiR-34a functions as a tumor suppressor in oral cancer through the inhibition of the Axl/Akt/GSK-3β pathway.Journal of dental sciences · 2024Article
- Nuclear translocation of Axl contributes to the malignancy of oral cancer cells.Journal of dental sciences · 2024Article
- TEAD transcription factor family emerges as a promising therapeutic target for oral squamous cell carcinoma.Frontiers in immunology · 2024Review
- A systematic review of preclinical studies evaluating the association between nicotine and the initiation and progression of cancer.Annals of translational medicine · 2023Review
- Changes in the Acetylcholinesterase Enzymatic Activity in Tumor Development and Progression.Cancers · 2023Review
- The expression of nicotinic acetylcholine receptor subunits and their associations with local immune cells and prognosis in oral squamous cell carcinoma.Cancer medicine · 2023Article
- The Effect of High Nicotine Dose on Maximum Anaerobic Performance and Perceived Pain in Healthy Non-Smoking Athletes: Crossover Pilot Study.International journal of environmental research and public health · 2023Article
- The risk profile of electronic nicotine delivery systems, compared to traditional cigarettes, on oral disease: a review.Frontiers in public health · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
Cigarette smoking is a significant risk factor for the development and progression of oral cancer. Previous studies have reported an association between nicotine and malignancy in oral cancer. Recent studies have also demonstrated that nicotine can induce endoplasmic reticulum (ER) stress in tumor cells. Binding immunoglobulin protein (BiP) acts as a master regulator of ER stress and is frequently overexpressed in oral cancer cell lines and tissues. However, the effect of nicotine on BiP in oral cancer is unknown. Therefore, this study aimed to evaluate the role of BiP and its underlying regulatory mechanisms in nicotine-induced oral cancer progression. Our results showed that nicotine significantly induced the expression of BiP in time- and dose-dependent manners in oral squamous cell carcinoma (OSCC) cells. In addition, BiP was involved in nicotine-mediated OSCC malignancy, and depletion of BiP expression remarkably suppressed nicotine-induced malignant behaviors, including epithelial-mesenchymal transition (EMT) change, migration, and invasion. In vivo, BiP silencing abrogated nicotine-induced tumor growth and EMT switch in nude mice. Moreover, nicotine stimulated BiP expression through the activation of the YAP-TEAD transcriptional complex. Mechanistically, we observed that nicotine regulated YAP nuclear translocation and its interaction with TEAD through α7-nAChR-Akt signaling, subsequently resulting in increased TEAD occupancy on the HSPA5 promoter and elevated promoter activity. These observations suggest that BiP is involved in nicotine-induced oral cancer malignancy and may have therapeutic potential in tobacco-related oral cancer.
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.