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HMGB1 knockdown increases MM cell vulnerability by regulating autophagy and DNA damage repair

Overview of attention for article published in Journal of Experimental & Clinical Cancer Research, August 2018
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3 tweeters

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Title
HMGB1 knockdown increases MM cell vulnerability by regulating autophagy and DNA damage repair
Published in
Journal of Experimental & Clinical Cancer Research, August 2018
DOI 10.1186/s13046-018-0883-3
Pubmed ID
Authors

Xing Guo, Donghua He, Enfan Zhang, Jing Chen, Qingxiao Chen, Yi Li, Li Yang, Yang, Yi Zhao, Gang Wang, Jingsong He, Zhen Cai

Abstract

With the development of novel therapeutic agents, the survival of multiple myeloma (MM) patients has much improved. However, the disease is incurable due to drug resistance. Previous studies have found that high-mobility group box 1 (HMGB1) is involved in inflammation, angiogenesis, DNA damage repair, and cancer invasion, progression, metastasis and drug resistance and that high HMGB1 expression is associated with poor MM prognosis, yet the role and mechanism of HMGB1 in MM remains unclear. Through gene expression and Oncomine database analyses, we found that HMGB1 is associated with a poor prognosis in MM patients. RNA interference together with gene array analysis, cell proliferation and apoptosis assays, autophagy detection assays, western blotting, and in vivo xenograft models were employed to evaluate the effect of HMGB1 and the mechanism involved in MM drug resistance. MM cell lines and primary MM samples were found to express high levels of HMGB1, which was negatively associated with the 3-year survival of MM patients. HMGB1 knockdown in MM cells enhanced the inhibitory effect of chemotherapy with dexamethasone (Dex) via apoptosis induction. Furthermore, downregulation of HMGB1 activated the mTOR pathway, inhibited autophagy and increased DNA damage induced by Dex by modulating expression of related genes. In vivo, xenograft models showed that after Dex treatment, the tumor burden of HMGB1-knockdown mice was decreased compared with that of control mice. Our research shows that HMGB1 participates in autophagy and DNA damage repair and that downregulation of HMGB1 enhances the sensitivity of MM cells to Dex, suggesting that HMGB1 may serve as a target for MM treatment.

Twitter Demographics

The data shown below were collected from the profiles of 3 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 27 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 7 26%
Student > Ph. D. Student 6 22%
Other 2 7%
Researcher 2 7%
Student > Master 1 4%
Other 1 4%
Unknown 8 30%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 19%
Medicine and Dentistry 4 15%
Pharmacology, Toxicology and Pharmaceutical Science 2 7%
Agricultural and Biological Sciences 2 7%
Immunology and Microbiology 2 7%
Other 4 15%
Unknown 8 30%

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 20 October 2018.
All research outputs
#7,697,142
of 13,647,261 outputs
Outputs from Journal of Experimental & Clinical Cancer Research
#259
of 966 outputs
Outputs of similar age
#131,719
of 265,821 outputs
Outputs of similar age from Journal of Experimental & Clinical Cancer Research
#1
of 1 outputs
Altmetric has tracked 13,647,261 research outputs across all sources so far. This one is in the 42nd percentile – i.e., 42% of other outputs scored the same or lower than it.
So far Altmetric has tracked 966 research outputs from this source. They receive a mean Attention Score of 2.7. This one has gotten more attention than average, scoring higher than 71% of its peers.
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 265,821 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 48th percentile – i.e., 48% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them