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Beclin-1 expression is retained in high-grade serous ovarian cancer yet is not essential for autophagy induction in vitro

Overview of attention for article published in Journal of Ovarian Research, August 2015
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Title
Beclin-1 expression is retained in high-grade serous ovarian cancer yet is not essential for autophagy induction in vitro
Published in
Journal of Ovarian Research, August 2015
DOI 10.1186/s13048-015-0182-y
Pubmed ID
Authors

Rohann J. M. Correa, Yudith Ramos Valdes, Trevor G. Shepherd, Gabriel E. DiMattia

Abstract

Autophagy is a conserved cellular self-digestion mechanism that can either suppress or promote cancer in a context-dependent manner. In ovarian cancer, prevalent mono-allelic deletion of BECN1 (a canonical autophagy-inducer) suggests that autophagy is impaired to promote carcinogenesis and that Beclin-1 is a haploinsufficient tumor suppressor. Nonetheless, autophagy is known to be readily inducible in ovarian cancer cells. We sought to clarify whether Beclin-1 expression is in fact disrupted in ovarian cancer and whether this impacts autophagy regulation. BECN1 expression levels were assessed using The Cancer Genome Atlas (TCGA) datasets from 398 ovarian high-grade serous cystadenocarcinomas (HGSC) and protein immunoblot data from HGSC samples obtained at our institution. Knockdown of BECN1 and other autophagy-related gene expression was achieved using siRNA in established human ovarian cancer cell lines (CaOV3, OVCAR8, SKOV3, and HeyA8) and a novel early-passage, ascites-derived cell line (iOvCa147-E2). LC3 immunoblot, autophagic flux assays, transmission electron microscopy and fluorescence microscopy were used to assess autophagy. We observed prevalent mono-allelic BECN1 gene deletion (76 %) in TCGA tumors, yet demonstrate for the first time that Beclin-1 protein expression remains relatively unaltered in these and additional samples generated at our institution. Surprisingly, efficient siRNA-mediated Beclin-1 knockdown did not attenuate autophagy induction, whereas knockdown of other autophagy-related genes blocked the process. Beclin-1 knockdown instead decreased cell viability without inducing apoptosis. Taken together, these data demonstrate that despite its sustained expression, Beclin-1 is dispensable for autophagy induction in ovarian tumor cells in vitro, yet may be retained to promote cell viability by a mechanism independent of autophagy or apoptosis regulation. Overall, this work makes novel observations about tumor expression of Beclin-1 and challenges the accepted understanding of its role in regulating autophagy in ovarian cancer.

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Mendeley readers

The data shown below were compiled from readership statistics for 32 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 32 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 7 22%
Student > Master 5 16%
Student > Ph. D. Student 4 13%
Other 3 9%
Researcher 2 6%
Other 7 22%
Unknown 4 13%
Readers by discipline Count As %
Medicine and Dentistry 7 22%
Biochemistry, Genetics and Molecular Biology 7 22%
Agricultural and Biological Sciences 4 13%
Pharmacology, Toxicology and Pharmaceutical Science 3 9%
Environmental Science 1 3%
Other 4 13%
Unknown 6 19%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. 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 05 August 2015.
All research outputs
#3,486,195
of 7,027,725 outputs
Outputs from Journal of Ovarian Research
#55
of 151 outputs
Outputs of similar age
#117,187
of 224,199 outputs
Outputs of similar age from Journal of Ovarian Research
#6
of 10 outputs
Altmetric has tracked 7,027,725 research outputs across all sources so far. This one is in the 28th percentile – i.e., 28% of other outputs scored the same or lower than it.
So far Altmetric has tracked 151 research outputs from this source. They receive a mean Attention Score of 2.9. This one is in the 48th percentile – i.e., 48% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 224,199 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 37th percentile – i.e., 37% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 10 others from the same source and published within six weeks on either side of this one. This one has scored higher than 4 of them.