MAPK/ERK-CBP-RFPL-3 Mediates Adipose-Derived Stem Cell-Induced Tumor Growth in Breast Cancer Cells by Activating Telomerase Reverse Transcriptase Expression

Li, Wenjie; Qian, Cheng; Ma, Fei; Liu, Meng; Sun, Xiaojun; Liu, Xu; Liu, Chunxiao; Chen, Zhenghua; Ma, Weichang; Liu, Jian; Xu, Haiqian; Yang, Zhenlin

doi:10.1155/2022/8540535

Cited by 5 publications

(3 citation statements)

References 33 publications

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“…These findings imply distinct responses to ADSC-derived conditioned medium between cancerous and non-cancerous breast cells ( 19 ). The triggering of MEK-ERK pathway in breast cancer cells co-culture with ADSCs was also indicated through nuclear CBP recruitment which later upregulates human telomerase reverse transcriptase transcription and telomerase activity ( 20 ). In another indirect co-culture of ADSCs and MDA-MB-231, and direct co-culture demonstrated no growth effect on breast cancer cell lines, but stimulated migration ( 21 ).…”

Section: Discussionmentioning

confidence: 99%

Breast fat grafting and cancer: a systematic review of the science behind enhancements and concerns

Valente,

Ely,

Kieling

et al. 2024

Transl Breast Cancer Res

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Background Autologous fat transfer (AFT) is gaining popularity in breast surgery, offering a natural-looking and minimally invasive approach for augmentation, reconstruction, and contouring. However, concerns about its impact on breast cancer necessitate an understanding of the interplay between transplanted adipose-derived stem cells (ADSCs) and the breast tissue microenvironment. Renowned for regeneration, ADSCs raise questions about their role in cancer promotion. This systematic review delves into the complex relationship between AFT and breast cancer, exploring how ADSCs may influence development, growth, and metastasis. Methods A systematic search of electronic databases, including PubMed, Embase, and BVS was conducted to identify relevant studies. The search strategy employed a combination of keywords, including “breast augmentation”, “fat grafting”, “breast enhancement”, “mammoplasty”, “cancer”, “neoplasm” and related terms. Two reviewers independently screened titles and abstracts. Full-text articles were then retrieved for further evaluation based on their potential contribution to the review objectives. Results Two hundred and forty records were identified. Among these, 104 duplicates were removed, resulting in 136 reports available for title and abstract screening. Subsequently, 54 papers were deemed potentially eligible for inclusion, and all reports were retrieved. Conclusions In vitro studies reveal ADSCs dual role in breast cancer, influencing proliferation, migration, and drug resistance through complex signaling pathways. Animal studies highlight distinct ADSC subpopulations impacting tumor growth via direct interactions and extracellular vesicle cargo. In vivo , ADSC-enriched fat grafting is generally safe, showing no increased cancer recurrence risk compared to other methods. Notably, cases of invasive breast carcinoma warrant special attention. ADSC-enriched fat grafts exhibit potential benefits in graft retention and survival rates. Despite promising evidence, further studies are needed to comprehensively understand the intricate relationship between ADSCs and breast cancer for optimized clinical applications and potential therapeutic innovations.

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Section: Discussionmentioning

confidence: 99%

Breast fat grafting and cancer: a systematic review of the science behind enhancements and concerns

Valente,

Ely,

Kieling

et al. 2024

Transl Breast Cancer Res

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“…Hu et al 25 found that FGFR1/MAPK was activated in lung cancer, inducing immune escape. Li et al 26 reported that the MAPK pathway upregulated telomerase activity, promoting breast cancer development. Additionally, Yi et al 27 demonstrated that the activated MAPK pathway induced mitochondrial fission and accelerated liver cancer progression.…”

Section: Discussionmentioning

confidence: 99%

SH3 domain‐binding kinase 1 promotes proliferation and inhibits apoptosis of cervical cancer via activating the Wnt/β‐catenin and Raf/ERK1/2 signaling pathways

Chen

Sun

Zhou

et al. 2023

Molecular Carcinogenesis

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SH3 domain‐binding kinase 1 (SBK1), is a member of the serine/threonine protein kinases family, and was confirmed to be upregulated in cervical cancer in our previous study. Nonetheless, the role of SBK1 in regulating cancer occurrence and development is unclear. In this study, the stable SBK1‐knockdown and ‐overexpressed cell models were constructed by plasmid transfection technology. Cell viability and growth were assessed through CCK‐8, colony formation, and BrdU methods. Cell cycle and apoptosis were analyzed by flow cytometry. The JC‐1 staining assay was used to explore mitochondrial membrane potential. The scratch and Transwell assays were used to evaluate the cell metastatic ability. The nude mice models were utilized to explore the SBK1 expression affecting tumor growth in vivo. Our research indicated a high expression of SBK1 both in tissues and cells of cervical cancer. The proliferative, migratory, as well as invasive capacities of cervical cancer cells, were suppressed, and apoptosis was enhanced after SBK1 silence, whereas SBK1 upregulation led to opposite results. In addition, Wnt/β‐catenin and Raf/ERK1/2 pathways were activated by SBK1 upregulation. Furthermore, downregulation of c‐Raf or β‐catenin, reversed the proliferation promotion and apoptosis inhibition effects in SBK1‐overexpressed cells. The same results were observed with the use of the specific Raf inhibitor. SBK1 overexpression also contributed to tumor growth in vivo. Overall, SBK1 played a vital role in cervical tumorigenesis via activating the Wnt/β‐catenin and Raf/ERK1/2 pathways.

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“…On this basis, previous studies have revealed that activation of the MAPK and PI3K signaling pathways are closely associated with tumorigenesis since they change the cellular microenvironment, promote tumor neovascularization and stimulate tumor cell proliferation ( 14 , 15 ). In addition, the MAPK/ERK signaling pathway has been found to have regulatory effect on cell differentiation in studies of breast cancer and rhabdomyosarcoma, which could potentially be the mechanism underlying the dedifferentiation of tumor cells in RR-DTC ( 16 , 17 ). However, investigations of the specific DEPs and signaling pathways associated with RR-DTC are lacking, and were therefore performed in the present study.…”

Section: Introductionmentioning

confidence: 99%

Proteomic analysis of radioiodine‑refractory differentiated thyroid cancer identifies CHI3L1 upregulation in association with dysfunction of the sodium‑iodine symporter

Deng

et al. 2022

Oncol Lett

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Radioiodine refractory differentiated thyroid cancer (RR-DTC) is the main factor adversely affecting the overall survival rate of patients with thyroid cancer. The aim of the present study was to investigate the underlying molecular mechanism of pathogenesis of RR-DTC and to explore novel therapeutic targets for clinical treatment. A proteomic analysis was performed using the tumor tissues of patients with RR-DTC. A total of 6 metastatic lymph nodes were collected during lymph node dissection, 3 from patients with RR-DTC and 3 from patients with papillary thyroid cancer. The expression of chitinase-3-like 1 (CHI3L1) and sodium-iodine symporter (NIS) in the tumor tissue was detected by immunohistochemistry (IHC). Western blotting was used to detect the expression of CHI3L1, phosphorylated (p)-MEK and p-ERK1/2 in PTC-K1 cells transfected with CHI3L1 overexpression vector. The proteomic analysis identified 665 differentially expressed proteins (DEPs), including 327 upregulated and 338 downregulated proteins in the RR-DTC group, which were enriched in 59 signaling pathways by Kyoto Encyclopedia of Genes and Genomes database analysis. In particular, CHI3L1 was demonstrated to be significantly upregulated in RR-DTC as evidenced by quantitative proteomic analysis and IHC. Western blotting suggested that the overexpression of CHI3L1 activated the MEK/ERK1/2 signaling pathway, which may lead to NIS dysfunction. In conclusion, the present study suggests that CHI3L1 is a potential molecular target for the radiotherapy of patients with RR-DTC.

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MAPK/ERK-CBP-RFPL-3 Mediates Adipose-Derived Stem Cell-Induced Tumor Growth in Breast Cancer Cells by Activating Telomerase Reverse Transcriptase Expression

Cited by 5 publications

References 33 publications

Breast fat grafting and cancer: a systematic review of the science behind enhancements and concerns

Breast fat grafting and cancer: a systematic review of the science behind enhancements and concerns

SH3 domain‐binding kinase 1 promotes proliferation and inhibits apoptosis of cervical cancer via activating the Wnt/β‐catenin and Raf/ERK1/2 signaling pathways

Proteomic analysis of radioiodine‑refractory differentiated thyroid cancer identifies CHI3L1 upregulation in association with dysfunction of the sodium‑iodine symporter

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