Evidence map›Paper›PMID 36900414›Full record

ArticleCancers2023

PKCθ Regulates Pituitary Adenoma Bone Invasion by Activating Osteoclast in NF-κB/IL-1β-Dependent Manner.

Quanji Wang, Zhuowei Lei, Zihan Wang, Qian Jiang, Zhuo Zhang, Xiaojin Liu, Biao Xing, Sihan Li, Xiang Guo, Yanchao Liu and 5 more

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In one paragraph

Article in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

10 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Quanji WangSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.
Zhuowei LeiDepartment of Orthopedics, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.
Zihan WangSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.
Qian JiangSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.
Zhuo ZhangSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.
Xiaojin LiuSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.ORCID 0000-0002-5649-2716
Biao XingSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.
Sihan LiSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.
Xiang GuoSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.
Yanchao LiuSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.
Xingbo LiSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.
Kai ShuSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.
Huaqiu ZhangSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.ORCID 0000-0003-3023-2040
Yimin HuangSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.
Ting LeiSino-German Neuro-Oncology Molecular Laboratory, Department of Neurosurgery, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, Jiefang Avenue 1095, Wuhan 430030, China.ORCID 0000-0003-3241-7567

Funding

National Nature Science Foundation of China 82173136
6 · The paper itself

Abstract

backgroundPituitary adenoma (PA) bone invasion results in adverse outcomes, such as reduced rates of complete surgical resection and biochemical remission as well as increased recurrence rates, though few studies have been conducted.

methodsWe collected clinical specimens of PAs for staining and statistical analysis. Evaluation of the ability of PA cells to induce monocyte-osteoclast differentiation by coculturing PA cells with RAW264.7 in vitro. An in vivo model of bone invasion was used to simulate the process of bone erosion and evaluate the effect of different interventions in alleviating bone invasion.

resultsWe found an overactivation of osteoclasts in bone-invasive PAs and concomitant aggregation of inflammatory factors. Furthermore, activation of PKCθ in PAs was established as a central signaling promoting PA bone invasion through the PKCθ/NF-κB/IL-1β pathway. By inhibiting PKCθ and blocking IL1β, we were able to significantly reverse bone invasion in an in vivo study. Meanwhile, we also found that celastrol, as a natural product, can obviously reduce the secretion of IL-1β as well as alleviate the progression of bone invasion.

conclusionsBy activating the PKCθ/NF-κB/IL-1β pathway, pituitary tumors are able to induce monocyte-osteoclast differentiation in a paracrine manner and promote bone invasion, which can be alleviated by celastrol.

Indexed as

bone invasioncelastrolmacrophageosteoclastspituitary adenomasPKCtheta

Identifiers

PMID36900414
PMCPMC10001016

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