Evidence map›Paper›PMID 33511766›Full record

ArticleJournal of cellular and molecular medicine2021

Parathyroid hormone type 1 receptor regulates osteosarcoma K7M2 Cell growth by interacting with angiotensinogen.

Shenglong Li, Fei Liu, Yi Pei, Yujin Dong, Yaohua Shang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
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

5 authors at 2 institutions in 1 country.

Shenglong LiDepartment of Bone and Soft Tissue Tumor Surgery, Liaoning Cancer Hospital & Institute, Cancer Hospital of China Medical University, Shenyang, China.ORCID 0000-0003-2244-1184
Fei LiuDepartment of Bone and Soft Tissue Tumor Surgery, Liaoning Cancer Hospital & Institute, Cancer Hospital of China Medical University, Shenyang, China.
Yi PeiDepartment of Bone and Soft Tissue Tumor Surgery, Liaoning Cancer Hospital & Institute, Cancer Hospital of China Medical University, Shenyang, China.
Yujin DongDepartment of Hand and Foot Surgery, Dalian Municipal Center Hospital Affiliated of Dalian Medical University, Dalian, China.
Yaohua ShangDepartment of Hand and Foot Surgery, Dalian Municipal Center Hospital Affiliated of Dalian Medical University, Dalian, China.
Liaoning Cancer Hospital & Institute · CNDalian Medical University · CN

Funding

Natural Science Foundation of Liaoning Province 2020-MS-058Shenyang young and middle-aged scientific and technological innovation talent support plan RC190456
6 · The paper itself

Abstract

This study aimed to determine the interactions between parathyroid hormone type 1 receptor (PTHR1) and angiotensinogen (AGT) and the effects of these agents on osteosarcoma (OS). We constructed a stably transfected mouse OS K7M2 cell line (shPTHR1- K7M2) using shRNA and knocked down AGT in these cells using siRNA-AGT. The transfection efficiency and expression of AGT, chemokine C-C motif receptor 3 (CCR3), and chemokine (C-C motif) ligand 9 (CCL9) were determined using real-time quantitative PCR. Cell viability and colony formation were assessed using Cell Counting Kit-8 and crystal violet staining, respectively. Cell apoptosis and cycle phases were assessed by flow cytometry, and cell migration and invasion were evaluated using Transwell assays. Interference with PTHR1 upregulated the expression of AGT and CCR3, and downregulated that of CCL9, which was further downregulated by AGT knockdown. Cell viability, migration, invasion and colony formation were significantly decreased, while cell apoptosis was significantly increased in shPTHR1-K7M2, compared with those in K7M2 cells (P < .05 for all). However, AGT knockdown further inhibited cell viability after 72 h of culture but promoted cell migration and invasion. PTHR1 interference decreased and increased the numbers of cells in the G0/G1 and G2/M phases, respectively, compared with those in K7M2 cells. Angiotensinogen knockdown increased the number of cells in the G0/G1 phase compared with that in the shPTHR1-K7M2 cells. Therefore, PTHR1 affects cell viability, apoptosis, migration, invasion and colony formation, possibly by regulating AGT/CCL9 in OS cells.

Indexed as

AngiotensinogenAnimalsApoptosisCell CycleCell Line, TumorCell MovementCell ProliferationCell SurvivalGene ExpressionGene Knockdown TechniquesMiceOsteosarcomaParathyroid HormoneProtein BindingReceptor, Parathyroid Hormone, Type 1RNA, Small InterferingAngiotensinogenParathyroid HormoneReceptor, Parathyroid Hormone, Type 1RNA, Small InterferingAGTCCL9osteosarcomaPTHR1

Identifiers

PMID33511766
PMCPMC7957183
OpenAlexW3126108603

What OpenQuestion holds

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LicenceCC BY
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.