| Title |
Autophagy suppresses proliferation of HepG2 cells via inhibiting glypican-3/wnt/β-catenin signaling
|
|---|---|
| Published in |
OncoTargets and therapy, January 2018
|
| DOI | 10.2147/ott.s150520 |
| Pubmed ID | |
| Authors |
Pei Hu, Bin Cheng, Yulin He, Zhiqiang Wei, Dongfang Wu, Zhongji Meng |
| Abstract |
Autophagy plays an important role in the growth and survival of hepatocellular carcinoma (HCC) cells through several target proteins or signaling pathways. Glypican-3 (GPC3) is a new reliable HCC marker, which is involved in tumor growth in HCC, primarily mediated by wnt/β-catenin signaling. The present study aimed to identify the role of autophagy in the proliferation of HepG2 cells through GPC3/wnt/β-catenin signaling. Results demonstrated that induction of autophagy by nutrition starvation and rapamycin treatment led to the downregulation of GPC3 expression in HepG2 cells, accompanied by the decreased expression of wnt downstream target genes (β-catenin, c-myc and cyclin D1). On the other hand, inhibition of autophagy by 3-methyl adenine (3-MA) could rescue rapamycin-directed downregulation of GPC3 and wnt/β-catenin target genes and augment the proliferation of HepG2 cells. Furthermore, interference of GPC3 by siRNA suppressed wnt/β-catenin signaling and attenuated 3-MA stimulation of HepG2 cell proliferation. More interestingly, the mRNA of GPC3 remained unchanged when the protein levels of GPC3 were decreased by autophagy activation, suggesting that induction of autophagy may accelerate the degradation of GPC3. These results suggest that autophagy suppresses proliferation of HepG2 cells partially by inhibition of GPC3/wnt/β-catenin signaling. |
X Demographics
The data shown below were collected from the profiles of 3 X users who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 3 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 3 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 12 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 12 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 4 | 33% |
| Student > Master | 4 | 33% |
| Researcher | 2 | 17% |
| Other | 1 | 8% |
| Unknown | 1 | 8% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 4 | 33% |
| Medicine and Dentistry | 3 | 25% |
| Pharmacology, Toxicology and Pharmaceutical Science | 1 | 8% |
| Agricultural and Biological Sciences | 1 | 8% |
| Chemistry | 1 | 8% |
| Other | 0 | 0% |
| Unknown | 2 | 17% |
Attention Score in Context
This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 02 February 2018.
All research outputs
#16,053,755
of 25,382,440 outputs
Outputs from OncoTargets and therapy
#887
of 3,016 outputs
Outputs of similar age
#255,125
of 449,550 outputs
Outputs of similar age from OncoTargets and therapy
#17
of 69 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. This one is in the 34th percentile – i.e., 34% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,016 research outputs from this source. They receive a mean Attention Score of 2.9. This one has gotten more attention than average, scoring higher than 67% of its peers.
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We're also able to compare this research output to 69 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 69% of its contemporaries.