Background: FAM83D is a spindle related protein and plays critical roles in mid-plate formation during mitosis. Aberrant FAM83D expression was reported in multiple cancers. Besides, it was observed that FAM83D was capable of promoting the proliferation and migration of normal or cancer cells in several tissues. Objective: we are aiming to update the latest advancement in FAM83D findings, and make a comprehensive review of FAM83D, in order to provide new perspectives for the research of FAM83D in tumors. Methods: Here, we summarized the latest published literatures of FAM83D in recent five years and categorized the research of FAM83D into lung cancer, digestive system cancers and female reproductive cancers. Then, we discussed the relationship of FAM83D and diagnosis, development and prognosis of multiple cancers, as well as the relevant in vitro intracellular underlying mechanisms. Conclusions: Up to now, FAM83D has been investigated in 9 types of cancers and its expression patterns found to tightly related to OS or DFS. Besides, most in vitro studies showed that FAM83D positively regulated cancer cell proliferations and differentiations. Furthermore, researches screened out several downstream targets and intracellular pathways of FAM83D as well as upstream regulatory factors. Prospectively, the biochemistry features of FAM83D protein and its potential as a biomarker of cancer diagnosis or therapy require more independent and rigorous studies.
| Published in | Biomedical Sciences (Volume 8, Issue 2) |
| DOI | 10.11648/j.bs.20220802.11 |
| Page(s) | 53-56 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2024. Published by Science Publishing Group |
FAM83D, Malignant Tumors, Tumor Biomarkers
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APA Style
Dekang Liu, Xiaowei Guan. (2022). FAM83D and Malignant Tumors: A Brief Literature Review. Biomedical Sciences, 8(2), 53-56. https://doi.org/10.11648/j.bs.20220802.11
ACS Style
Dekang Liu; Xiaowei Guan. FAM83D and Malignant Tumors: A Brief Literature Review. Biomed. Sci. 2022, 8(2), 53-56. doi: 10.11648/j.bs.20220802.11
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Download@article{10.11648/j.bs.20220802.11,
author = {Dekang Liu and Xiaowei Guan},
title = {FAM83D and Malignant Tumors: A Brief Literature Review},
journal = {Biomedical Sciences},
volume = {8},
number = {2},
pages = {53-56},
doi = {10.11648/j.bs.20220802.11},
url = {https://doi.org/10.11648/j.bs.20220802.11},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.bs.20220802.11},
abstract = {Background: FAM83D is a spindle related protein and plays critical roles in mid-plate formation during mitosis. Aberrant FAM83D expression was reported in multiple cancers. Besides, it was observed that FAM83D was capable of promoting the proliferation and migration of normal or cancer cells in several tissues. Objective: we are aiming to update the latest advancement in FAM83D findings, and make a comprehensive review of FAM83D, in order to provide new perspectives for the research of FAM83D in tumors. Methods: Here, we summarized the latest published literatures of FAM83D in recent five years and categorized the research of FAM83D into lung cancer, digestive system cancers and female reproductive cancers. Then, we discussed the relationship of FAM83D and diagnosis, development and prognosis of multiple cancers, as well as the relevant in vitro intracellular underlying mechanisms. Conclusions: Up to now, FAM83D has been investigated in 9 types of cancers and its expression patterns found to tightly related to OS or DFS. Besides, most in vitro studies showed that FAM83D positively regulated cancer cell proliferations and differentiations. Furthermore, researches screened out several downstream targets and intracellular pathways of FAM83D as well as upstream regulatory factors. Prospectively, the biochemistry features of FAM83D protein and its potential as a biomarker of cancer diagnosis or therapy require more independent and rigorous studies.},
year = {2022}
}
TY - JOUR T1 - FAM83D and Malignant Tumors: A Brief Literature Review AU - Dekang Liu AU - Xiaowei Guan Y1 - 2022/04/26 PY - 2022 N1 - https://doi.org/10.11648/j.bs.20220802.11 DO - 10.11648/j.bs.20220802.11 T2 - Biomedical Sciences JF - Biomedical Sciences JO - Biomedical Sciences SP - 53 EP - 56 PB - Science Publishing Group SN - 2575-3932 UR - https://doi.org/10.11648/j.bs.20220802.11 AB - Background: FAM83D is a spindle related protein and plays critical roles in mid-plate formation during mitosis. Aberrant FAM83D expression was reported in multiple cancers. Besides, it was observed that FAM83D was capable of promoting the proliferation and migration of normal or cancer cells in several tissues. Objective: we are aiming to update the latest advancement in FAM83D findings, and make a comprehensive review of FAM83D, in order to provide new perspectives for the research of FAM83D in tumors. Methods: Here, we summarized the latest published literatures of FAM83D in recent five years and categorized the research of FAM83D into lung cancer, digestive system cancers and female reproductive cancers. Then, we discussed the relationship of FAM83D and diagnosis, development and prognosis of multiple cancers, as well as the relevant in vitro intracellular underlying mechanisms. Conclusions: Up to now, FAM83D has been investigated in 9 types of cancers and its expression patterns found to tightly related to OS or DFS. Besides, most in vitro studies showed that FAM83D positively regulated cancer cell proliferations and differentiations. Furthermore, researches screened out several downstream targets and intracellular pathways of FAM83D as well as upstream regulatory factors. Prospectively, the biochemistry features of FAM83D protein and its potential as a biomarker of cancer diagnosis or therapy require more independent and rigorous studies. VL - 8 IS - 2 ER -
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