ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
Stathmin in pancreatic neuroendocrine neoplasms: a marker of proliferation and PI3K signaling.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Stathmin guides personalized therapy in oral squamous cell carcinoma.Cancer science · 2020Trial
- Article
- Stathmin 1 across neuroendocrine neoplasms: biological, pathological and translational insights.Frontiers in endocrinology · 2026Review
- Evaluation of Stathmin Expression in Different Oral Squamous Lesions: A Retrospective Cross-Sectional Study.International journal of dentistry · 2026Article
- The role of cell cycle-related genes in the tumorigenesis of adrenal and thyroid neuroendocrine tumors.Heliyon · 2025Review
- Cell cycle-related genes associate with sensitivity to hydrogen peroxide-induced toxicity.Redox biology · 2022Article
- Hypoxia destroys the microstructure of microtubules and causes dysfunction of endothelial cells via the PI3K/Stathmin1 pathway.Cell & bioscience · 2019Article
- Stathmin 1 expression predicts prognosis and benefits from adjuvant chemotherapy in patients with gallbladder carcinoma.Oncotarget · 2017Article
- Molecular strategies in the management of bronchopulmonary and thymic neuroendocrine neoplasms.Journal of thoracic disease · 2017Review
- Stathmin overexpression is associated with growth, invasion and metastasis of lung adenocarcinoma.Oncotarget · 2017Article
- Advances in β cell replacement and regeneration strategies for treating diabetes.The Journal of clinical investigation · 2016Review
- Stathmin-dependent molecular targeting therapy for malignant tumor: the latest 5 years' discoveries and developments.Journal of translational medicine · 2016Review
- Elevated STMN1 promotes tumor growth and invasion in endometrial carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- miR-193b directly targets STMN1 and inhibits the malignant phenotype in colorectal cancer.American journal of cancer research · 2016Article
- Stathmin1 increases radioresistance by enhancing autophagy in non-small-cell lung cancer cells.OncoTargets and therapy · 2016Article
- Research Resource: A Dual Proteomic Approach Identifies Regulated Islet Proteins During β-Cell Mass Expansion In Vivo.Molecular endocrinology (Baltimore, Md.) · 2016Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosome 1p35-36, which encodes tumor suppressors and mitotic checkpoint control genes, is commonly altered in human malignancies. One gene at this locus, stathmin 1 (STMN1), is involved in cell cycle progression and metastasis. We hypothesized that increased STMN1 expression may play a role in pancreatic neuroendocrine neoplasm (pNEN) malignancy. We investigated stathmin copy number variation, mRNA, and protein expression using PCR-Taqman Copy Number Assays, Q-PCR, Western blot, and immunohistochemistry. A mechanistic role for stathmin in proliferation was assessed in the BON cell line under growth-restrictive conditions and siRNA silencing. Furthermore, its role in PI3K signaling pathway activation was evaluated using pharmacological inhibitors. mRNA (p = 0.0001) and protein (p < 0.05) were overexpressed in pNENs. Expression was associated with pNEN tumor extension (p < 0.05), size (p < 0.01), and Ki67 expression (p < 0.01). Serum depletion decreased Ki67 expression (p < 0.01) as well as Ser38 phosphorylation (p < 0.05) in BON cells. STMN1 knockdown (siRNA) decreased proliferation (p < 0.05), and PI3K inhibitors directly inhibited proliferation via stathmin inactivation (dephosphorylation p < 0.01). We identified that stathmin was overexpressed and associated with pathological parameters in pancreatic NENs. We postulate that STMN1 overexpression and phosphorylation result in a loss of cell cycle mitotic checkpoint control and may render tumors amenable to PI3K inhibitory therapy.
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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.