Mitochondrial stress adaptation promotes resistance to aromatase inhibitor in human breast cancer cells via ROS/calcium up-regulated amphiregulin–estrogen receptor loop signaling

Wang, Sheng-Fan; Chang, Yuh Lih; Tzeng, Yen‐Dun Tony; Wu, Cheng‐Li; Wang, Yuanzhong; Tseng, Ling Ming; Chen, Shiuan

doi:10.1016/j.canlet.2021.09.043

Cited by 16 publications

(14 citation statements)

References 90 publications

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“…might increase intracellular levels of reactive oxygen species (ROS) and calcium, which promotes gene transcription, translation and secretion of AREG by mitonuclear retrograde signaling. 23 We detected the effects of BAPTA-AM (a cell membrane-permeable calcium chelator) and NAC (N-Acetylcysteine, a ROS inhibitor) on mRNA levels of EREG and AREG under treatment of tigecycline. Results showed that BAPTA-AM and NAC could decrease the expression of EREG and AREG which were stimulated by the treatment of tigecycline ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Sustained activation of EGFR-ERK1/2 signaling limits the response to tigecycline-induced mitochondrial respiratory deficiency in liver cancer

Zhou

Wang

et al. 2023

eBioMedicine

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Section: Resultsmentioning

confidence: 99%

Sustained activation of EGFR-ERK1/2 signaling limits the response to tigecycline-induced mitochondrial respiratory deficiency in liver cancer

Zhou

Wang

et al. 2023

eBioMedicine

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“…7 Moreover, mitochondrial stress adaptation-increased intracellular levels of reactive oxygen species (ROS) and intracellular calcium are shown to induce alpha-amphiregulin (AREG) expression and secretion, while the up-regulation of AREG activates the PI3K/ Akt/mTOR pathway. 33 Additionally, membrane stretch-mediated Ca2+ influx through Piezo1 is an important trigger for phosphorylation of AKT mediated upregulation of pulmonary arterial endothelial cells. 34 Thus, in contrast to our results, intracellular Ca2+ may be regulate the AKT pathway in part via Piezo1 in melanoma cells.…”

Section: Discussionmentioning

confidence: 99%

Mechanically activated ion channel Piezo1 contributes to melanoma malignant progression through AKT/mTOR signaling

Zhang

Cao

Gong

et al. 2022

Cancer Biology & Therapy

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Melanoma is a highly aggressive cancer that can metastasize at early stage. The aim of this study is to clarify the role of Piezo1 and its potential mechanism in regulating the malignant phenotypes of melanoma. In the present study, we first showed that Piezo1 was abnormally expressed in melanoma, which accelerated the malignant progression by activating AKT/mTOR signaling. Firstly, we found that Piezo1 was upregulated in melanoma and associated with poor survival. Additionally, Piezo1 knockdown significantly weakened intracellular calcium signal and viability of melanoma cells. Furthermore, Piezo1 knockdown inhibited the transendothelial migration and invasion in vitro, as well as metastasis in vivo. Mechanistically, we found that Piezo1 activated AKT/mTOR signaling to maintain malignant phenotypes of melanoma. Therefore, Piezo1 acts as an oncogene in melanoma cells and provides a novel candidate for melanoma diagnosis and treatment.

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“…By binding to EGFR, AREG activates various downstream signaling pathways, such as the MAPK/ERK, PI3K/AKT, STAT, and mTOR pathways, mediating cell survival, proliferation, and differentiation, among other functions 5 . Lee's 35 study found that upregulated AREG‐EGFR crosstalk activated the ERK pathways in breast cancer cells. AREG‐EGFR activated ERK1/2 in epithelial cells 16 .…”

Section: Discussionmentioning

confidence: 99%

AREG is involved in scleral remodeling in form‐deprivation myopia via the ERK1/2‐MMP‐2 pathway

She

Shi

et al. 2022

The FASEB Journal

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Previous studies have found that amphiregulin (AREG) may participate in eye elongation during the development of myopia, but the mechanism remains unclear. Here, we tested tear concentrations of AREG in adults and detected the role of AREG in scleral remodeling in form‐deprivation myopia (FDM) in guinea pigs. We found the tear concentrations of AREG in myopes were significantly higher than those in emmetropes using enzyme‐linked immunosorbent assay (ELISA). Tear concentrations of AREG were negatively correlated with spherical equivalent refraction and positively correlated with axial length (AL) and AL/corneal radii. We then used RNAi, DNA transfection and PD98059 treatments to determine the effects of AREG on extracellular signal‐regulated kinase 1/2 (ERK1/2) and matrix metalloprotease‐2 (MMP‐2) in primary scleral fibroblasts (SFs). The hypothesis was further verified via loss‐ and gain‐of‐function experiments by intravitreal application of anti‐AREG antibody (anti‐AR) or AREG in form‐deprivation eyes in guinea pigs. Immunofluorescence assay was used for cell type identification. Western‐blot and q‐PCR were used for the detection of relative expressions. Transmission electron microscopy was performed for posterior scleral observation. In vitro, we found AREG overexpression increased phospho‐ERK1/2 and MMP‐2 expression, while depletion of AREG inhibited their expressions. PD98059 (an effective ERK1/2 inhibitor) inhibited AREG‐induced MMP‐2 upregulation. In vivo, we found anti‐AR treatments suppressed FDM by inhibiting scleral remodeling, while AREG treatments promoted FDM. Our results suggest that AREG in tear fluids can serve as a potential biomarker in myopes. AREG is involved in scleral remodeling through the ERK1/2‐MMP‐2 pathway. AREG is a potential target for myopia control.

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Mitochondrial stress adaptation promotes resistance to aromatase inhibitor in human breast cancer cells via ROS/calcium up-regulated amphiregulin–estrogen receptor loop signaling

Cited by 16 publications

References 90 publications

Sustained activation of EGFR-ERK1/2 signaling limits the response to tigecycline-induced mitochondrial respiratory deficiency in liver cancer

Sustained activation of EGFR-ERK1/2 signaling limits the response to tigecycline-induced mitochondrial respiratory deficiency in liver cancer

Mechanically activated ion channel Piezo1 contributes to melanoma malignant progression through AKT/mTOR signaling

AREG is involved in scleral remodeling in form‐deprivation myopia via the ERK1/2‐MMP‐2 pathway

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