Reticulocalbin 1 is required for proliferation and migration of non‐small cell lung cancer cells regulated by osteoblast‐conditioned medium

Fu, Haijing; Chen, Rui; Wang, Yue; Xu, Yang; Xia, Chun; Zhang, Bing

doi:10.1111/jcmm.17040

Cited by 11 publications

(12 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 9 , 23 , 24 , 25 , 26 , 27 , 28 RCN1 and COL11A1 are highly expressed in lung cancer and promote lung cancer cell proliferation, migration, and invasion. 29 , 30 RHOC is one of the three isoforms of the Rho family of GTPases and MMP14 is one of the matrix metalloproteinase family members, which are widely involved in cell movement. 25 , 31 TNFSF11, also named RANKL, is a critical regulator for cancer bone metastases.…”

Section: Resultsmentioning

confidence: 99%

“…In addition to GPX8, the others have been reported to involve in cancer metastasis 9,23–28 . RCN1 and COL11A1 are highly expressed in lung cancer and promote lung cancer cell proliferation, migration, and invasion 29,30 . RHOC is one of the three isoforms of the Rho family of GTPases and MMP14 is one of the matrix metalloproteinase family members, which are widely involved in cell movement 25,31 .…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Glutathione peroxidase 8 expression on cancer cells and cancer‐associated fibroblasts facilitates lung cancer metastasis

Yuan

Jiang

et al. 2022

MedComm

View full text Add to dashboard Cite

Lung cancer is the leading cause of cancer death worldwide, of which lung adenocarcinoma (LUAD) is the most common subtype. Metastasis is the major cause of poor prognosis and mortality for lung cancer patients, which urgently needs great efforts to be further explored. Herein, glutathione peroxidase 8 (GPX8) was identified as a novel potential pro‐metastatic gene in LUAD metastatic mice models from GEO database. GPX8 was highly expressed in tumor tissues, predicting poor prognosis in LUAD patients. Knockdown of GPX8 inhibited LUAD metastasis in vitro and in vivo, while it did not obviously affect tumor growth. Knockdown of GPX8 decreased the levels of p‐FAK and p‐Paxillin and disturbed the distribution of focal adhesion. Furthermore, GPX8 was overexpressed in cancer‐associated fibroblast (CAF) and associated with CAF infiltration in tumor microenvironment of lung cancer. GPX8 silence on fibroblasts suppressed lung cancer cell migration in the coculture system. BRD2 and RRD4 were the potential transcriptionally regulators for GPX8. Bromodomain extra‐terminal inhibitor JQ1 downregulated GPX8 expression and suppressed lung cancer cell migration. Our findings indicate that highly expressed GPX8 in lung cancer cells and fibroblasts functions as a pro‐metastatic factor in lung cancer. JQ1 is identified as a potential inhibitor against GPX8‐mediated lung cancer metastasis.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Glutathione peroxidase 8 expression on cancer cells and cancer‐associated fibroblasts facilitates lung cancer metastasis

Yuan

Jiang

et al. 2022

MedComm

View full text Add to dashboard Cite

show abstract

“…Recent evidences indicate that non-canonical signaling is important in oncogenesis via the interaction with PI3K, mTORC2, AKT, MAPK pathway, and HIF-1α in the cytoplasm and nuclear ( Ayaz and Osborne, 2014 ; Li et al, 2016 ; Zou et al, 2019 ; Qin et al, 2020 ). The MAPK pathway is activated in lung cancer and plays a critical role in the development and progression of cancer ( Fu et al, 2021 ; Hu et al, 2021 ; Jain et al, 2021 ; Shin et al, 2021 ). Our results showed that Notch4 silencing downregulated phosphorylation of ERK, JNK, and P38.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia Activates Notch4 via ERK/JNK/P38 MAPK Signaling Pathways to Promote Lung Adenocarcinoma Progression and Metastasis

Li¹,

Cao²,

Zhao³

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Hypoxia contributes to the progression and metastasis of lung adenocarcinoma (LUAD). However, the specific underlying molecular mechanisms have not been fully elucidated. Here we report that Notch4 is upregulated in lung tissue from lung cancer patients. Functionally, Hypoxia activates the expressions of Delta-like 4 and Notch4, resulting in the excessive proliferation and migration of LUAD cells as well as apoptotic resistance. Notch4 silencing reduced ERK, JNK, and P38 activation. Meanwhile, Notch4 overexpression enhanced ERK, JNK, and P38 activation in LUAD cells. Furthermore, Notch4 exerted pro-proliferation, anti-apoptosis and pro-migration effects on LUAD cells that were partly reversed by the inhibitors of ERK, JNK, and p38. The binding interaction between Notch4 and ERK/JNK/P38 were confirmed by the co-immunoprecipitation assay. In vivo study revealed that Notch4 played a key role in the growth and metastasis of LUAD using two xenograft models. This study demonstrates that hypoxia activates Notch4-ERK/JNK/P38 MAPK signaling pathways to promote LUAD cell progression and metastasis.

show abstract

“…Recent studies have shown that RCN1 plays a tumor-promoting role in tumor progression (9,10,12,23). However, the role of RCN1 in ESCC has not yet been studied.…”

Section: Discussionmentioning

confidence: 99%

“…There have been reports of RCN1 protein dysregulation in a variety of diseases, including cardiovascular disease, neuromuscular disease, and tumors (6-8). In recent years, RCN1 has received widespread attention due to its important role in tumorigenesis and progression (9)(10)(11)(12)(13). For example, in prostate cancer cells, downregulation of RCN1 promoted apoptosis and necrosis of cancer cells (13); in non-small cell lung cancer, high expression of the RCN1 protein was found to be signi cantly associated with poor prognosis in non-small cell lung cancer patients, and inhibition of RCN1 was shown to reduce proliferation, migration, and invasion of lung adenocarcinoma cells (12).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of RCN1 inhibits esophageal squamous cell carcinoma progression and M2 macrophage polarization

Guo,

Su,

et al. 2023

Preprint

View full text Add to dashboard Cite

Background: Reticulocalbin 1 (RCN1) is a calcium-binding protein involved in the regulation of calcium homeostasis in the endoplasmic reticulum. The aim of this study was to explore the clinical value and biological role of RCN1 in esophageal squamous cell carcinoma (ESCC). In addition, we also investigated the effect of RCN1 on the polarization of tumor-associated macrophages (TAMs). Methods: The GSE53625 dataset from the Gene Expression Omnibus database was used to analyze the expression of RCN1 mRNA and the relationship with clinical value and immune cell infiltration. Immunohistochemistry was used to validate the expression of RCN1 and its correlation with clinicopathological characteristics. Subsequently, transwell and cell scratch assays were conducted to evaluate the migration and invasion abilities of ESCC cells. The expression levels of epithelial–mesenchymal transition (EMT)-related proteins were detected using Western blotting, while flow cytometry and Western blotting were employed to detect cell apoptosis. Additionally, qRT-PCR and Western blotting were utilized to evaluate the role of RCN1 in macrophage polarization. Results: RCN1is significantly upregulated in ESCC tissues and is closely associated with lymphatic metastasis and a poor prognosis; it is an independent prognostic factor for ESCC patients. Knockdown of RCN1 significantly inhibits migration, invasion, and EMT of ESCC cells, and promotes cell apoptosis. In addition, RCN1 downregulation inhibited the polarization of M2 macrophages. Conclusion: RCN1is upregulated in ESCC patients and is negatively correlated with patient prognosis. Knocking down RCN1 can inhibit the progression of ESCC cells and polarization of M2 macrophages. RCN1 could serve as a potential diagnostic and prognostic indicator for ESCC, and targeting RCN1 is a very promising therapeutic target.

show abstract

Reticulocalbin 1 is required for proliferation and migration of non‐small cell lung cancer cells regulated by osteoblast‐conditioned medium

Cited by 11 publications

References 48 publications

Glutathione peroxidase 8 expression on cancer cells and cancer‐associated fibroblasts facilitates lung cancer metastasis

Glutathione peroxidase 8 expression on cancer cells and cancer‐associated fibroblasts facilitates lung cancer metastasis

Hypoxia Activates Notch4 via ERK/JNK/P38 MAPK Signaling Pathways to Promote Lung Adenocarcinoma Progression and Metastasis

Downregulation of RCN1 inhibits esophageal squamous cell carcinoma progression and M2 macrophage polarization

Contact Info

Product

Resources

About