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This article is original for Translational Medicine.
Please indicate the source when reprinting.
Author: Ashley Introduction: Recent studies have shown that breast cancer stem cells (BCSCs) secretomes autonomously oppress stem cell populations
.
Co-implantation with BCSCs decreased tumor-initiating capacity but increased concomitant cancer cell metastasis, with DKK1 identified as a key factor in this function secreted by BCSCs
.
The promotion of differentiation by DKK1 is essential for the metastatic growth of disseminated tumor cells
.
In contrast, DKK1 inhibitors substantially alleviated metastatic burden by inhibiting dormant metastatic cells
.
This study deciphers the role of cancer stem cell (CSCs)-regulated phenotypic plasticity in metastatic colonization and provides a therapeutic approach to limit metastatic growth
.
Cancer stem cells (CSCs) are key drivers behind the progression of malignant cancers with self-renewal, high metastases and resistance to therapy
.
As cancer progresses, cancer cells exhibit phenotypic plasticity between stem-like and differentiated subpopulations, each of which can recreate the composition of the parental cells
.
However, the mechanisms and functions of this plasticity remain largely unknown
.
In a study "Cancer stem cell regulated phenotypic plasticity protects metastasized cancer cells from ferroptosis" published in Nature Communications, a research team led by Professor Zhu Tao from the Chinese University of Science and Technology of China (USTC), Chinese Academy of Sciences, uncovered the phenotypes regulated by CSCs The role of plasticity in metastatic colonization
.
https:// We designed an in vitro co-culture system and an in vivo co-implantation system
.
Based on these systems, they discovered the ability of breast cancer stem cells (BCSCs) to suppress themselves through the BSCS-derived secretome
.
Through screening, bioluminescence imaging and other means, they also found that DKK1 plays a pivotal role in the secretome
.
DKK1 was identified as a key molecule that autonomously reduces the population of CSCs and subsequently promotes breast cancer metastatic colonization
.
Further experiments showed that this autonomous restraint of BCSCs could prompt a large number of dormant disseminated tumor cells (DTCs) to exit from dormancy after reaching distant sites, and then achieve metastatic colonization
.
However, small-molecule inhibitors of DKK1 can achieve almost complete blockade of lung metastasis in many models of BCSCs metastasis
.
Ferroptosis is a non-apoptotic cell death process that results from metabolic abnormalities and lipid peroxidation
.
Compared with primary breast cancer, lung metastatic cancer cells are subject to higher oxidative and iron stress
.
The researchers revealed that highly aggressive CSCs have relatively high concentrations in lung metastases, and CSCs can secrete DKK1, which inhibits CSCs
.
As CSCs are highly sensitive to ferroptosis, DKK1 secreted by CSCs protects cells in lung metastases from ferroptosis and thus metastatic growth
.
The findings of this study shed light on the role of CSCs-regulated phenotypic plasticity in metastatic colonization and provide a new therapeutic approach to effectively inhibit metastasis
.
Reference: https://medicalxpress.
com/news/2022-04-ways-limit-cancer-growth.
html Note: This article aims to introduce the progress of medical research and cannot be used as a reference for treatment plans
.
For health guidance, please go to a regular hospital for treatment
.
Recommendation·Event Click the text to view the details.
March 30th 19:00-21:00 Online Seminar on Frontier Progress of Proteomics and Prospects of Innovative Technologies March 31st 19:00-21:00 Sharing Global Technology Online| Oncology Precision Diagnosis Innovation and Development Webinar April 13th 19:00-21:00 Online Innovative Drug R&D and Research and Development Salon (coming soon) April 14th 15:00-16:20 Online based on real-time living cells Imaging-based targeted tumor therapy (to be announced soon) April 20, 09:00-18:00 How to improve the efficiency of new macromolecular drug research and development from basic experiments (to be announced soon)
Please indicate the source when reprinting.
Author: Ashley Introduction: Recent studies have shown that breast cancer stem cells (BCSCs) secretomes autonomously oppress stem cell populations
.
Co-implantation with BCSCs decreased tumor-initiating capacity but increased concomitant cancer cell metastasis, with DKK1 identified as a key factor in this function secreted by BCSCs
.
The promotion of differentiation by DKK1 is essential for the metastatic growth of disseminated tumor cells
.
In contrast, DKK1 inhibitors substantially alleviated metastatic burden by inhibiting dormant metastatic cells
.
This study deciphers the role of cancer stem cell (CSCs)-regulated phenotypic plasticity in metastatic colonization and provides a therapeutic approach to limit metastatic growth
.
Cancer stem cells (CSCs) are key drivers behind the progression of malignant cancers with self-renewal, high metastases and resistance to therapy
.
As cancer progresses, cancer cells exhibit phenotypic plasticity between stem-like and differentiated subpopulations, each of which can recreate the composition of the parental cells
.
However, the mechanisms and functions of this plasticity remain largely unknown
.
In a study "Cancer stem cell regulated phenotypic plasticity protects metastasized cancer cells from ferroptosis" published in Nature Communications, a research team led by Professor Zhu Tao from the Chinese University of Science and Technology of China (USTC), Chinese Academy of Sciences, uncovered the phenotypes regulated by CSCs The role of plasticity in metastatic colonization
.
https:// We designed an in vitro co-culture system and an in vivo co-implantation system
.
Based on these systems, they discovered the ability of breast cancer stem cells (BCSCs) to suppress themselves through the BSCS-derived secretome
.
Through screening, bioluminescence imaging and other means, they also found that DKK1 plays a pivotal role in the secretome
.
DKK1 was identified as a key molecule that autonomously reduces the population of CSCs and subsequently promotes breast cancer metastatic colonization
.
Further experiments showed that this autonomous restraint of BCSCs could prompt a large number of dormant disseminated tumor cells (DTCs) to exit from dormancy after reaching distant sites, and then achieve metastatic colonization
.
However, small-molecule inhibitors of DKK1 can achieve almost complete blockade of lung metastasis in many models of BCSCs metastasis
.
Ferroptosis is a non-apoptotic cell death process that results from metabolic abnormalities and lipid peroxidation
.
Compared with primary breast cancer, lung metastatic cancer cells are subject to higher oxidative and iron stress
.
The researchers revealed that highly aggressive CSCs have relatively high concentrations in lung metastases, and CSCs can secrete DKK1, which inhibits CSCs
.
As CSCs are highly sensitive to ferroptosis, DKK1 secreted by CSCs protects cells in lung metastases from ferroptosis and thus metastatic growth
.
The findings of this study shed light on the role of CSCs-regulated phenotypic plasticity in metastatic colonization and provide a new therapeutic approach to effectively inhibit metastasis
.
Reference: https://medicalxpress.
com/news/2022-04-ways-limit-cancer-growth.
html Note: This article aims to introduce the progress of medical research and cannot be used as a reference for treatment plans
.
For health guidance, please go to a regular hospital for treatment
.
Recommendation·Event Click the text to view the details.
March 30th 19:00-21:00 Online Seminar on Frontier Progress of Proteomics and Prospects of Innovative Technologies March 31st 19:00-21:00 Sharing Global Technology Online| Oncology Precision Diagnosis Innovation and Development Webinar April 13th 19:00-21:00 Online Innovative Drug R&D and Research and Development Salon (coming soon) April 14th 15:00-16:20 Online based on real-time living cells Imaging-based targeted tumor therapy (to be announced soon) April 20, 09:00-18:00 How to improve the efficiency of new macromolecular drug research and development from basic experiments (to be announced soon)
