Evidence map›Paper›PMID 30122899›Full record

ArticleDrug design, development and therapy2018

Sinomenine inhibits the growth of melanoma by enhancement of autophagy via PI3K/AKT/mTOR inhibition.

Zheng Sun, Lingling Zheng, Xujun Liu, Wenlong Xing, Xinhai Liu

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Synthesis and growth inhibitory activity of sinomenine derivatives against cervical cancer SiHa cells through targeting the AKT-CyclinD1-p21/p27 pathway.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
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  6. Doramectin Induces Apoptosis in B16 Melanoma Cells.Anti-cancer agents in medicinal chemistry · 2025
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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

5 authors at 2 institutions in 1 country.

Zheng SunDepartment of Dermatology and Venereology, Beijing Luhe Hospital, Capital Medical University, Beijing, People's Republic of China.
Lingling ZhengDepartment of Dermatology and Venereology, Beijing Luhe Hospital, Capital Medical University, Beijing, People's Republic of China.
Xujun LiuDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, People's Republic of China.
Wenlong XingDepartment of Cardiovasology, Beijing Chinese Medicine Hospital, Capital Medical University, Beijing, People's Republic of China.
Xinhai LiuDepartment of Plastic Surgery, Beijing Luhe Hospital, Capital Medical University, Beijing, People's Republic of China, 3418139937@qq.com.
Beijing Luhe Hospital Affiliated to Capital Medical University · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMelanoma is a common skin tumor in adults with high metastasis and mortality rates. Thus, finding a better effective approach to treat melanoma has become very urgent. Sinomenine (SIN), the major active compound of PURPOSE: This study aimed to explore the effects of SIN on melanoma in vitro and in vivo, in addition to exploring the underlying mechanism.

methodsMouse melanoma cell B16-F10 treated by SIN was analyzed by CCK8 assay and flow cytometry. Melanoma xenograft model was then established by subcutaneously injection with B16-F10 cells. Tumor growth was measured by immunohistochemistry. To further investigate the relative mechanism, the autophagy and PI3K/Akt/mTOR pathway were examined by immunofluorescence and Western blot.

resultsOur results revealed that SIN dose dependently inhibited the proliferation of B16-F10 cells in vitro and attenuated melanoma growth in vivo. In addition, SIN treatment promoted the apoptosis of B16-F10 cells in a dose-dependent manner, as demonstrated by the increase in apoptotic cells, Bax/Bcl-2 ratio, and caspase-3 activity. Moreover, preconditioning with SIN dramatically enhanced autophagy activity by increasing Beclin-1 and LC3II/LC3I expression, in addition to decreasing p62 expression and augmenting the number of LC3 puncta, in B16-F10 cells. More importantly, autophagy inhibitor chloroquine partly abolished SIN's effects on cell growth and apoptosis. Furthermore, our results showed that SIN-triggered activation of autophagy was mediated by PI3K/Akt/mTOR signaling pathway.

conclusionOur study has identified a novel function of SIN and provided a molecular basis for potential applications of SIN in the treatment of melanoma and other cancers.

Indexed as

Phosphoinositide-3 Kinase InhibitorsAnimalsApoptosisAutophagyCell Line, TumorHumansMelanoma, ExperimentalMiceMice, Inbred BALB CMorphinansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesMorphinansPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktsinomenineTOR Serine-Threonine KinasesautophagymelanomaPI3K/Akt/mTORsinomenine

Identifiers

PMID30122899
PMCPMC6084074
OpenAlexW2887672801

What OpenQuestion holds

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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.