Evidence map›Paper›PMID 30854129›Full record

ArticleJournal of Cancer2019

Lyn Kinase Promotes the Proliferation of Malignant Melanoma Cells through Inhibition of Apoptosis and Autophagy via the PI3K/Akt Signaling Pathway.

Qianqian Zhang, Xianguang Meng, Guojing Qin, Xiaotong Xue, Ningning Dang

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Functional Profiling of Soft Tissue Sarcoma Using Mechanistic Models.International journal of molecular sciences · 2023
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
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  11. Article
  12. Article
  13. Article
  14. Cancer management and research · 2020
    Article
  15. 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 1 institution in 1 country.

Qianqian ZhangDepartment of Dermatology, Jinan Central Hospital affiliated to Shandong University, Jinan, Shandong Province, China.
Xianguang MengDepartment of Dermatology, Jinan Central Hospital affiliated to Shandong University, Jinan, Shandong Province, China.
Guojing QinDepartment of Dermatology, Jinan Central Hospital affiliated to Shandong University, Jinan, Shandong Province, China.
Xiaotong XueDepartment of Dermatology, Jinan Central Hospital affiliated to Shandong University, Jinan, Shandong Province, China.
Ningning DangDepartment of Dermatology, Jinan Central Hospital affiliated to Shandong University, Jinan, Shandong Province, China.
Jinan Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma is a malignant tumor of cutaneous melanocytes that is characterized by high grade malignancy, rapid progression and high mortality. Thus far, its specific etiological mechanism has been unclear. In this study, we discovered that Lyn kinase expression was up-regulated in melanoma tissues and cells. The function of Lyn was determined by knocking down its expression with a lentivirus containing Lyn shRNA and upregulating its expression with pcDNA3.1-Lyn in the melanoma cell lines M14 and A375. The results showed that Lyn knockdown could significantly inhibit the proliferation, migration and invasiveness through its inhibition of apoptosis and autophagy via the PI3K/Akt pathway in melanoma cell lines. This was further confirmed by treatment with PI3K inhibitor BEZ235. Up-regulation of Lyn promoted the expression of p-Akt and Cyclin D1. Additionally, we investigated the effects of Lyn inhibitor Bafetinib on melanoma cells and the results were consistent with Lyn knockdown. Collectively, our results indicated that Lyn plays a carcinogenic role in multiple cellular functions during melanoma development through regulating apoptosis and autophagy via the PI3K/Akt pathway and may be a valuable potential target for the clinical treatment of melanoma.

Indexed as

autophagyLynmelanomaPI3K/Aktproliferation

Identifiers

PMID30854129
PMCPMC6400685
OpenAlexW2911296504

What OpenQuestion holds

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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.