Evidence map›Paper›PMID 32110051›Full record

ArticleOncoTargets and therapy2020

Knockdown of FOXO6 Inhibits Glycolysis and Reduces Cell Resistance to Paclitaxel in HCC Cells via PI3K/Akt Signaling Pathway.

Xixiang Yu, Xixi Gao, Xiaoping Mao, Zhenjing Shi, Bangxuan Zhu, Linqin Xie, Shaodan Di, Limin Jin

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. 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 23% 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, 22 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.

Xixiang YuWenzhou Medical University, Wenzhou No. 3 Clinical College, Wenzhou, Zhejiang Province, People's Republic of China.
Xixi GaoQingyuan County People's Hospital, Qingyuan, Zhejiang Province, People's Republic of China.
Xiaoping MaoThe Third Affiliated Hospital of Wenzhou Medical University, Ruian, Zhejiang Province, People's Republic of China.
Zhenjing ShiThe Third Affiliated Hospital of Wenzhou Medical University, Ruian, Zhejiang Province, People's Republic of China.
Bangxuan ZhuWenzhou Medical University, Wenzhou No. 3 Clinical College, Wenzhou, Zhejiang Province, People's Republic of China.
Linqin XieWenzhou Medical University, Wenzhou No. 3 Clinical College, Wenzhou, Zhejiang Province, People's Republic of China.
Shaodan DiWenzhou Medical University, Wenzhou No. 3 Clinical College, Wenzhou, Zhejiang Province, People's Republic of China.
Limin JinThe Third Affiliated Hospital of Wenzhou Medical University, Ruian, Zhejiang Province, People's Republic of China.
Wenzhou Medical University · CNRuian People's Hospital · CNQingzhou City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposePrevious studies have reported that FOXO6 is highly expressed in hepatocellular carcinoma (HCC) tissues and is associated with the prognosis of HCC patients. However, little research has been carried out to explore the role of FOXO6 in glycolysis of HCC cells and paclitaxel resistance. Today, along with the increasing incidence and mortality of HCC, chemotherapy resistance of HCC also poses a serious challenge. Therefore, this study was set out to investigate the effect of FOXO6 on glycolysis and cytotoxicity of paclitaxel in HCC cells and its potential mechanism. PATIENTS AND

methodsThe levels of FOXO6 mRNA and protein were detected by qRT-PCR and Western blot, respectively. In addition, paclitaxel-resistant cell lines of HCC cells were established, whose activity was assessed by CCK-8 assay, among which the invasion ability was assessed by Transwell and the apoptosis rate by flow cytometry. What is more, glycolysis levels were evaluated by measuring glucose consumption and lactic acid production, and the protein levels of p-PI3K and p-protein kinase B (Akt) were determined by Western blot.

resultsCompared with normal human hepatocytes, FOXO6 was highly expressed in HCC cells, which was of high real value for HCC. FOXO6 knockdown inhibited the proliferation and invasion and induced apoptosis of HCC cells. In addition, FOXO6 knockdown suppressed glycolysis, reversed resistance to chemotherapy in Hep3B/PTX cells and inactivated PI3K and Akt proteins, thus inhibiting the PI3K/Akt signaling pathway. Furthermore, it was found that when activated by 740Y-P, PI3K/Akt signaling pathway could resist the effects of FOXO6 knockdown on the cytotoxicity and glycolysis of paclitaxel in HCC cells. Vice versa, inhibition of PI3K/Akt pathway by LY294002 could resist the effect of FOXO6 overexpression on chemotherapy, cytotoxicity and glycolysis of HCC cells.

conclusionFOXO6 knockdown can inhibit glycolysis of HCC cells and reduce their resistance to chemotherapy by inhibiting the PI3K/Akt signaling pathway, which may be a new target for the treatment of HCC.

Indexed as

drug resistanceFOXO6glycolysishepatocellular carcinoma cellspaclitaxelPI3K/Akt signaling pathway

Identifiers

PMID32110051
PMCPMC7037170
OpenAlexW3007494073

What OpenQuestion holds

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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.