<scp>BAIAP2L1</scp> accelerates breast cancer progression and chemoresistance by activating <scp>AKT</scp> signaling through binding with ribosomal protein L3

Deng, Ning; Zhang, Xiupeng; Zhang, Yong

doi:10.1111/cas.15632

Cited by 9 publications

(6 citation statements)

References 37 publications

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“…Previous research has suggested that IRTKS, as a scaffold protein, is of great importance in modulation of actin movement and cell structure [16,17]. IRTKS has also been found to play a tumor-promoting role in a variety of tumors, including hepatocellular carcinoma [11], gastric cancer [18], pancreatic cancer [19],breast cancer [20]and lung cancer [21]. In the above cancers, IRTKS is actively related to their carcinogenesis, so it is probable that IRTKS acts as an oncogene.…”

Section: Discussionmentioning

confidence: 99%

IRTKS Contributes to the Malignant Progression of Cervical Cancer Cells

Zhang,

Yi,

Zhang

et al. 2024

Preprint

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Background Cervical cancer (CC), one of the most aggressive tumors in women, has high risk rates of recurrence and metastasis. It is essential to study the key genes and proteins involved in CC development. IRTKS, a member of the IRSp53 family, has been reported as a tumor promoter in gastric and breast cancers. However, the biological significance of IRTKS in CC is still unclear. The purpose of this study was to explore the biological function of IRTKS in CC cells in vitro, and the effect of IRTKS on tumorigenesis in vivo. Materials and Methods Siha and Hela cells were treated with si-RNA and plasmids. Cell proliferation and motility were analyzed using proliferation and transwell assays, respectively. The expression of EMT-related proteins was determined by western blot. Results IRTKS was highly expressed in CC. IRTKS contributes to the proliferation of CC cells in vitro and in vivo. Furthermore, IRTKS facilitated the migration and invasion of CC cells and modulated epithelial-mesenchymal transition. Conclusion IRTKS plays a crucial role in CC tumorigenesis, suggesting it can be a potential key gene in new therapeutic strategies for CC.

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Section: Discussionmentioning

confidence: 99%

IRTKS Contributes to the Malignant Progression of Cervical Cancer Cells

Zhang,

Yi,

Zhang

et al. 2024

Preprint

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“…The role of ALB in BC plasma-derived sEV is still unclear, but low expressions of ALB in serum were found to be associated with poor BC prognosis [54]. Despite the previous discovery of COL1A1 [55], EEF1A2 [56,57], and RPL3 [58] as metastasis-related proteins in BC and CSN1S1 [59], C5 [60], and C7 [61] as BC prognosis-related proteins, the function or biomarker potential of these proteins within sEVs remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Comparison Study of Small Extracellular Vesicle Isolation Methods for Profiling Protein Biomarkers in Breast Cancer Liquid Biopsies

Lee,

Ni,

Wasinger

et al. 2023

IJMS

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Small extracellular vesicles (sEVs) are an important intercellular communicator, participating in all stages of cancer metastasis, immunity, and therapeutic resistance. Therefore, protein cargoes within sEVs are considered as a superior source for breast cancer (BC) biomarker discovery. Our study aimed to optimise the approach for sEV isolation and sEV proteomic analysis to identify potential sEV protein biomarkers for BC diagnosis. sEVs derived from BC cell lines, BC patients’ plasma, and non-cancer controls were isolated using ultracentrifugation (UC), a Total Exosome Isolation kit (TEI), and a combined approach named UCT. In BC cell lines, the UC isolates showed a higher sEV purity and marker expression, as well as a higher number of sEV proteins. In BC plasma samples, the UCT isolates showed the highest proportion of sEV-related proteins and the lowest percentage of lipoprotein-related proteins. Our data suggest that the assessment of both the quantity and quality of sEV isolation methods is important in selecting the optimal approach for the specific sEV research purpose, depending on the sample types and downstream analysis.

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“…All participants provided written informed consent, and the study was conducted in accordance with the principles of the Declaration of Helsinki. Detailed descriptions of patient information have been described previously [ 40 ] and can be found in Additional file 1.…”

Section: Methodsmentioning

confidence: 99%

TMEM120B strengthens breast cancer cell stemness and accelerates chemotherapy resistance via β1-integrin/FAK-TAZ-mTOR signaling axis by binding to MYH9

Hu,

Cao,

Wang

et al. 2024

Breast Cancer Res

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Background Breast cancer stem cell (CSC) expansion results in tumor progression and chemoresistance; however, the modulation of CSC pluripotency remains unexplored. Transmembrane protein 120B (TMEM120B) is a newly discovered protein expressed in human tissues, especially in malignant tissues; however, its role in CSC expansion has not been studied. This study aimed to determine the role of TMEM120B in transcriptional coactivator with PDZ-binding motif (TAZ)-mediated CSC expansion and chemotherapy resistance. Methods Both bioinformatics analysis and immunohistochemistry assays were performed to examine expression patterns of TMEM120B in lung, breast, gastric, colon, and ovarian cancers. Clinicopathological factors and overall survival were also evaluated. Next, colony formation assay, MTT assay, EdU assay, transwell assay, wound healing assay, flow cytometric analysis, sphere formation assay, western blotting analysis, mouse xenograft model analysis, RNA-sequencing assay, immunofluorescence assay, and reverse transcriptase-polymerase chain reaction were performed to investigate the effect of TMEM120B interaction on proliferation, invasion, stemness, chemotherapy sensitivity, and integrin/FAK/TAZ/mTOR activation. Further, liquid chromatography–tandem mass spectrometry analysis, GST pull-down assay, and immunoprecipitation assays were performed to evaluate the interactions between TMEM120B, myosin heavy chain 9 (MYH9), and CUL9. Results TMEM120B expression was elevated in lung, breast, gastric, colon, and ovarian cancers. TMEM120B expression positively correlated with advanced TNM stage, lymph node metastasis, and poor prognosis. Overexpression of TMEM120B promoted breast cancer cell proliferation, invasion, and stemness by activating TAZ-mTOR signaling. TMEM120B directly bound to the coil-coil domain of MYH9, which accelerated the assembly of focal adhesions (FAs) and facilitated the translocation of TAZ. Furthermore, TMEM120B stabilized MYH9 by preventing its degradation by CUL9 in a ubiquitin-dependent manner. Overexpression of TMEM120B enhanced resistance to docetaxel and doxorubicin. Conversely, overexpression of TMEM120B-∆CCD delayed the formation of FAs, suppressed TAZ-mTOR signaling, and abrogated chemotherapy resistance. TMEM120B expression was elevated in breast cancer patients with poor treatment outcomes (Miller/Payne grades 1–2) than in those with better outcomes (Miller/Payne grades 3–5). Conclusions Our study reveals that TMEM120B bound to and stabilized MYH9 by preventing its degradation. This interaction activated the β1-integrin/FAK-TAZ-mTOR signaling axis, maintaining stemness and accelerating chemotherapy resistance.

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BAIAP2L1 accelerates breast cancer progression and chemoresistance by activating AKT signaling through binding with ribosomal protein L3

Cited by 9 publications

References 37 publications

IRTKS Contributes to the Malignant Progression of Cervical Cancer Cells

IRTKS Contributes to the Malignant Progression of Cervical Cancer Cells

Comparison Study of Small Extracellular Vesicle Isolation Methods for Profiling Protein Biomarkers in Breast Cancer Liquid Biopsies

TMEM120B strengthens breast cancer cell stemness and accelerates chemotherapy resistance via β1-integrin/FAK-TAZ-mTOR signaling axis by binding to MYH9

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