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X Demographics
Mendeley readers
Attention Score in Context
| Title |
SALL1 functions as a tumor suppressor in breast cancer by regulating cancer cell senescence and metastasis through the NuRD complex
|
|---|---|
| Published in |
Molecular Cancer, April 2018
|
| DOI | 10.1186/s12943-018-0824-y |
| Pubmed ID | |
| Authors |
Chunling Ma, Fang Wang, Bing Han, Xiaoli Zhong, Fusheng Si, Jian Ye, Eddy C. Hsueh, Lynn Robbins, Susan M. Kiefer, Yanping Zhang, Pamela Hunborg, Mark A. Varvares, Michael Rauchman, Guangyong Peng |
| Abstract |
SALL1 is a multi-zinc finger transcription factor that regulates organogenesis and stem cell development, but the role of SALL1 in tumor biology and tumorigenesis remains largely unknown. We analyzed SALL1 expression levels in human and murine breast cancer cells as well as cancer tissues from different types of breast cancer patients. Using both in vitro co-culture system and in vivo breast tumor models, we investigated how SALL1 expression in breast cancer cells affects tumor cell growth and proliferation, metastasis, and cell fate. Using the gain-of function and loss-of-function strategies, we dissected the molecular mechanism responsible for SALL1 tumor suppressor functions. We demonstrated that SALL1 functions as a tumor suppressor in breast cancer, which is significantly down-regulated in the basal like breast cancer and in estrogen receptor (ER), progesterone receptor (PR) and epidermal growth factor receptor 2 (HER2) triple negative breast cancer patients. SALL1 expression in human and murine breast cancer cells inhibited cancer cell growth and proliferation, metastasis, and promoted cell cycle arrest. Knockdown of SALL1 in breast cancer cells promoted cancer cell growth, proliferation, and colony formation. Our studies revealed that tumor suppression was mediated by recruitment of the Nucleosome Remodeling and Deacetylase (NuRD) complex by SALL1, which promoted cancer cell senescence. We further demonstrated that the mechanism of inhibition of breast cancer cell growth and invasion by SALL1-NuRD depends on the p38 MAPK, ERK1/2, and mTOR signaling pathways. Our studies indicate that the developmental control gene SALL1 plays a critical role in tumor suppression by recruiting the NuRD complex and thereby inducing cell senescence in breast cancer cells. |
X Demographics
The data shown below were collected from the profiles of 8 X users who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| India | 1 | 13% |
| United Kingdom | 1 | 13% |
| Unknown | 6 | 75% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 4 | 50% |
| Practitioners (doctors, other healthcare professionals) | 3 | 38% |
| Science communicators (journalists, bloggers, editors) | 1 | 13% |
Mendeley readers
The data shown below were compiled from readership statistics for 40 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 40 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Bachelor | 8 | 20% |
| Student > Ph. D. Student | 5 | 13% |
| Student > Doctoral Student | 4 | 10% |
| Researcher | 4 | 10% |
| Student > Master | 3 | 8% |
| Other | 6 | 15% |
| Unknown | 10 | 25% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 12 | 30% |
| Agricultural and Biological Sciences | 6 | 15% |
| Medicine and Dentistry | 6 | 15% |
| Pharmacology, Toxicology and Pharmaceutical Science | 2 | 5% |
| Chemical Engineering | 1 | 3% |
| Other | 1 | 3% |
| Unknown | 12 | 30% |
Attention Score in Context
This research output has an Altmetric Attention Score of 3. 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 31 July 2019.
All research outputs
#13,075,788
of 23,041,514 outputs
Outputs from Molecular Cancer
#793
of 1,734 outputs
Outputs of similar age
#159,731
of 329,529 outputs
Outputs of similar age from Molecular Cancer
#8
of 20 outputs
Altmetric has tracked 23,041,514 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 1,734 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.7. This one has gotten more attention than average, scoring higher than 53% 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 329,529 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 50% of its contemporaries.
We're also able to compare this research output to 20 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 60% of its contemporaries.