Evidence map›Paper›PMID 31168297›Full record

ArticleCancer cell international2019

Targeting Akt by SC66 triggers GSK-3β mediated apoptosis in colon cancer therapy.

Yeying Liu, Yuan Huang, Jie Ding, Nannan Liu, Shuang Peng, Jiangang Wang, Feng Wang, Yingjie Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Yeying LiuDepartment of Health Management, The Third Xiangya Hospital, Central South University, College of Biology, Hunan University, No. 1, Denggao Road, Changsha, China.
Yuan HuangDepartment of Health Management, The Third Xiangya Hospital, Central South University, College of Biology, Hunan University, No. 1, Denggao Road, Changsha, China.
Jie Ding3Department of Emergency Surgery, The Second Military Medical University, Shanghai, China.
Nannan LiuDepartment of Health Management, The Third Xiangya Hospital, Central South University, College of Biology, Hunan University, No. 1, Denggao Road, Changsha, China.
Shuang PengDepartment of Health Management, The Third Xiangya Hospital, Central South University, College of Biology, Hunan University, No. 1, Denggao Road, Changsha, China.
Jiangang WangDepartment of Health Management, The Third Xiangya Hospital, Central South University, College of Biology, Hunan University, No. 1, Denggao Road, Changsha, China.
Feng Wang2Department of Gastroenterology, The Tenth People's Hospital of Shanghai, Tongji University, Shanghai, China.
Yingjie ZhangDepartment of Health Management, The Third Xiangya Hospital, Central South University, College of Biology, Hunan University, No. 1, Denggao Road, Changsha, China.ORCID 0000-0002-9207-2364
Central South University · CNSecond Military Medical University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundColon cancer is one of the three common malignant tumors, with lower 5 years survival rate. Akt is an important therapeutic target, while SC66 is a novel allosteric AKT inhibitor, which enhances the therapeutic effect in several types of cancer. However, the molecular mechanisms of targeting AKT by SC66 during colon cancer therapy are not well understood.

methodsThe biological role of GSK-3β in colon cancer growth suppression induced by SC66 was detected in vitro and in vivo. Hoechst 33342 and crystal violet staining were used to determine whether targeting AKT affected apoptosis and cell proliferation. The CCK8 assay was utilized to analyze cell viability. The expression levels of Akt, GSK-3β, Bax, Bcl-xL, p53 and PUMA were measured by immune blotting. Xenograft mouse model was established to study the antitumor effect of SC66 in vivo.

resultsOur results show that SC66 induced significantly colon cancer cell apoptosis, accompanied with Akt inactivation. After AKT inhibition, activated GSK-3β interacted with Bax directly, leading to Bax oligomerization and activation. Knocking down GSK-3β abrogated SC66-triggered Bax activation and apoptosis, which was enhanced by over-expressed GSK-3β. In addition, the expression level of Bcl-xL was down-regulated while p53 had no function during SC66-induced apoptosis. Furthermore, colon cancer growth was suppressed by SC66 therapy in vivo.

conclusionTaken together, these data indicated that the novel small molecule AKT inhibitor SC66 shows visible antitumor effects via the AKT/GSK-3β/Bax axis in vitro and in vivo. Our results provide a rational basis for the development of targeting-GSK-3β, which may serve as a potential biomarker and yield meaningful benefits for colon cancer patients in the future.

Indexed as

AKTBcl-xLColon cancerGSK-3βSC66

Identifiers

PMID31168297
PMCPMC6509835
OpenAlexW2947284273

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.