Evidence map›Paper›PMID 33416096›Full record

ArticleInternational journal of molecular medicine2021

CDKN2A (p16INK4A) affects the anti‑tumor effect of CDK inhibitor in somatotroph adenomas.

Yiyuan Chen, Zhenye Li, Qiuyue Fang, Hongyun Wang, Chuzhong Li, Hua Gao, Yazhuo Zhang

RetractedErratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in International journal of molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 30% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Clinical significance and prospective mechanism of increased CDKN2A expression in small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Article
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Yiyuan ChenDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, P.R. China.
Zhenye LiDepartment of Neurosurgery, Beijing Tiantan Hospital Affiliated to Capital Medical University, Beijing 100070, P.R. China.
Qiuyue FangDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, P.R. China.
Hongyun WangDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, P.R. China.
Chuzhong LiDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, P.R. China.
Hua GaoDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, P.R. China.
Yazhuo ZhangDepartment of Cell Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, P.R. China.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The altered cell cycle is associated with aberrant growth factor signaling in somatotroph adenoma, which is the primary cause of acromegaly. The aim of the present study was to investigate the pathological role of the INK4 family and evaluate the effectiveness of CDK4 inhibitor, palbociclib, in somatotroph adenoma. RNA‑Seq, RT‑PCR, and immunohistochemistry were applied to measure the levels and correlations of the INK4 family with angiogenesis, CDKs, EMT, and therapeutic targets. MTS, flow cytometry, and ELISA were used to investigate the bio‑activity in GH3 and GT1‑1 cell lines after palbociclib treatment. Compared with lactotroph adenoma, gonadotroph adenoma, and corticotroph adenoma, somatotroph samples demonstrated higher expression of CDKN2A and SSTR2 but a lower expression of EGFR, CDK4, and CDH2 (P<0.05). CDKN2A positively correlates with SSTR2, and negatively with CDK4, EGFR, and CDH2. Patients with lower CDKN2A had larger tumor size (P=0.016) and more invasive potential (P=0.023). Palbociclib inhibited cell proliferation, induced G1 phase arrest, reduced GH/IGF‑1 secretion of GH3 and GT1‑1 cell lines (P<0.05), and had a more prominent role in GH3 cells (P<0.05). CDKN2A inhibited the bio‑activity by modulating CDK4, and high CDKN2A predicted the insensitivity to CDK4 inhibitor, palbociclib, in somatotroph adenoma patients. In summary, the present study shows CDKN2A inhibited the bio‑activity by modulating CDK4, and high CDKN2A predicts the insensitivity to CDK4 inhibitor, Palbociclib, in somatotroph adenoma patients.

Indexed as

AdenomaCyclin-Dependent Kinase 4Growth Hormone-Secreting Pituitary AdenomaAdultAntineoplastic AgentsCell Line, TumorCyclin-Dependent Kinase Inhibitor p16FemaleG1 Phase Cell Cycle CheckpointsHumansMaleMiddle AgedPiperazinesPyridinesAntineoplastic AgentsCDK4 protein, humanCDKN2A protein, humanCyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p16palbociclibPiperazinesPyridinesCDK4CDKN2A (p16INK4A)INK4 familypalbociclibsomatotroph adenomas

Identifiers

PMID33416096
PMCPMC7797444
OpenAlexW3108789544

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.