S100A11 regulates renal carcinoma cell proliferation, invasion, and migration via the EGFR/Akt signaling pathway and E-cadherin

Liu, Lin; Miao, Long; Liu, Yang; Qi, Aihua; Xie, Ping; Chen, Jiacun; Zhu, Hongguang

doi:10.1177/1010428317705337

Cited by 17 publications

(17 citation statements)

References 31 publications

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“…Consistent with cell proliferation assay, stably down‐regulating S100A11 using shRNA inhibited colony formation in RBE and HCCC 9810 cells (Figure E‐G, K‐M) and colony formation increased obviously in RBE and HCCC 9810 cells after transfected with the S100A11 overexpression vector (Figure H‐J, N‐P). Cell cycle assay showed RBE cells and HCCC9810 cells were both arrested at G1 phase after knockdown of S100A11, which was consistent with other literature findings (Supplementary Figure S3A‐D). This result just happened to explain why proliferation was inhibited after silencing S100A11 in RBE and HCCC9810 cells.…”

Section: Resultssupporting

confidence: 91%

“…Our results were in accordance with previous reports, which demonstrated that S100A11 promoted cell proliferation of breast cancer and pancreatic carcinoma . Additionally, cell cycle assay revealed cells were arrested in G1 phase in both RBE and HCC9810 cells after silencing S100A11, which was consistent with the research in renal carcinoma cells . Collectively, we can draw a conclusion that cells in G1 phase are unable transit to S phase after silencing S100A11.…”

Section: Discussionsupporting

confidence: 93%

“…This suggested that if ICC patients had high expression of S100A11 should be classified to be a high-risk population because of their possible poorer OS and RFS. S100A11 deficiency has been reported to arrest cells in the G0/G1 phase 20 and inhibit TGF-β induced epithelial-to-mesenchymal transition 11,29 and suppress tumor cell proliferation. 30 In this present study, cell proliferation and colony formation were inhibited in RBE cells and HCCC9810 cells after silencing S100A11 with siRNA or shRNA, but these effects were reversed after transfected S100A11 overexpression vector.…”

Section: Figurementioning

confidence: 99%

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S100A11 promotes cell proliferation via P38/MAPK signaling pathway in intrahepatic cholangiocarcinoma

Zhang

Gan

Jing

et al. 2018

Molecular Carcinogenesis

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S100A11 is reported to associate with progression and poor prognosis in several tumors. We previously reported that S100A11 was highly expressed in intrahepatic cholangiocarcinoma (ICC) cells and promoted TGF-β1-induced EMT through SMAD2/3 signaling pathway. Here, we explored the prognostic role of S100A11 on ICC patients and preliminary molecular mechanisms how S100A11 regulated ICC cell proliferation. Our results showed that S100A11 was obviously increased in ICC tumor tissues. High expression of S100A11 was closely correlated with lymph node metastasis (LNM) and TNM stage and was an independent risk factor for patients' overall survival (OS) and recurrence-free survival (RFS). The nomograms comprising LNM and S100A11 achieved better predictive accuracy compared with TNM staging system for OS and RFS prediction. Silencing S100A11 significantly suppressed RBE cells and HCCC9810 cells proliferation, colony formation, and activation of P38/mitogen-activated protein kinase (MAPK) signaling pathway in vitro and inhibited tumor growth in vivo. In contrast, the overexpression of S100A11 in RBE cells and HCCC9810 cells achieved the opposite results. S100A11-induced proliferation was abolished after treatment with P38 inhibitor. Our findings suggest S100A11/P38/MAPK signaling pathway may be a potential therapeutic target for ICC patients.

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Section: Resultssupporting

confidence: 91%

Section: Discussionsupporting

confidence: 93%

Section: Figurementioning

confidence: 99%

See 1 more Smart Citation

S100A11 promotes cell proliferation via P38/MAPK signaling pathway in intrahepatic cholangiocarcinoma

Zhang

Gan

Jing

et al. 2018

Molecular Carcinogenesis

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“…[13][14][15] In contrast, as the bioinformatic results suggest, 4T1 cells cultured in a sparse environment were more likely to be connected to metabolism events, especially for lipids or cholesterol, which may associated with cancer-cell growth or survival. [29][30][31][32] Hypoxia, which usually happens in tumour sites where cancer cells have a high speed of proliferation marked with Ki67 upregulated, can induce the expression of S100A11 to regulate the motility of smooth muscle cell. JAM-1 was decreased in samples from dense cultures, which was verified by a western blot.…”

Section: Figurementioning

confidence: 99%

Proteomic analysis of the effects of cell culture density on the metastasis of breast cancer cells

Guo

Mixin

Lan

et al. 2019

Cell Biochemistry & Function

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Cancer cell progression and proliferation increase cell density, resulting in changes to the tumour site, including the microenvironment. What is not known is if increased cell density influences the aggressiveness of cancer cells, especially their proliferation, migration, and invasion capabilities. In this study, we found that dense cell culture enhances the aggressiveness of the metastatic cancer cell lines, 4T1 and ZR-75-30, by increasing their proliferation, migration, and invasion capabilities. However, a less metastatic cell line, MCF-7, did not show an increase in aggressiveness, following dense cell culture conditions. We conducted a differential proteomic analysis on 4T1 cells cultured under dense or sparse conditions and identified an increase in expression for proteins involved in migration, including focal adhesion, cytoskeletal reorganization, and transendothelial migration. In contrast, 4T1 cells grown under sparse conditions had higher expression levels for proteins involved in metabolism, including lipid and phospholipid binding, lipid and cholesterol transporter activity, and protein binding.These results suggest that the high-density tumour microenvironment can cause a change in cellular behaviour, leading towards more aggressive cancers.Significance of the study: Metastasis of cancer cells is an obstacle to the clinical treatment of cancer. We found that dense cultures made metastatic cancer cells more potent in terms of proliferation, migration, and invasion. The proteomic and bioinformatic analyses provided some valuable clues for further intensive studies about the effects of cell density on cancer cell aggressiveness, which were associated with events such as pre-mRNA splicing and RNA transport, focal adhesion and cytoskeleton reorganization, ribosome biogenesis, and transendothelial migration, or associated with proteins, such as JAM-1 and S100A11. This investigation gives us new perspectives to investigate the metastasis mechanisms related to the microenvironment of tumour sites.

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“…The binding of EGF to an EGF receptor (EGFR) can promote cell survival and proliferation (Cohen et al ., ; Prenzel et al ., ). In addition, EGFR signaling also favors cell differentiation, migration, and invasion in vitro (Abd El‐Rehim et al ., ; Liu et al ., ; da Rosa et al ., ). In contrast to TGF‐β signaling, EGF/EGFR signaling predominantly functions as a promoter in tumorigenesis (Arteaga and Engelman, ).…”

Section: Introductionmentioning

confidence: 99%

TGF‐β transactivates EGFR and facilitates breast cancer migration and invasion through canonical Smad3 and ERK/Sp1 signaling pathways

et al. 2018

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Transforming growth factor‐beta (TGF‐β) functions as a potent proliferation inhibitor and apoptosis inducer in the early stages of breast cancer, yet promotes cancer aggressiveness in the advanced stages. The dual effect of TGF‐β on cancer development is known as TGF‐β paradox, and the remarkable functional conversion of TGF‐β is a pivotal and controversial phenomenon that has been widely investigated for decades. This phenomenon may be attributed to the cross talk between TGF‐β signaling and other pathways, including EGF receptor (EGFR) signaling during cancer progression. However, the underlying mechanism by which TGF‐β shifts its role from a tumor suppressor to a cancer promoter remains elusive. In this study, TGF‐β is positively correlated with EGFR expression in breast cancer tissues, and a functional linkage is observed between TGF‐β signaling and EGFR transactivation in breast cancer cell lines. TGF‐β promotes the migration and invasion abilities of breast cancer cells, along with the increase in EGFR expression. EGFR is also essential for TGF‐β‐induced enhancement of these abilities of breast cancer cells. Canonical Smad3 signaling and ERK/Sp1 signaling pathways mediate TGF‐β‐induced EGFR upregulation. Hence, our study provided insights into a novel mechanism by which TGF‐β supports breast cancer progression.

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S100A11 regulates renal carcinoma cell proliferation, invasion, and migration via the EGFR/Akt signaling pathway and E-cadherin

Cited by 17 publications

References 31 publications

S100A11 promotes cell proliferation via P38/MAPK signaling pathway in intrahepatic cholangiocarcinoma

S100A11 promotes cell proliferation via P38/MAPK signaling pathway in intrahepatic cholangiocarcinoma

Proteomic analysis of the effects of cell culture density on the metastasis of breast cancer cells

TGF‐β transactivates EGFR and facilitates breast cancer migration and invasion through canonical Smad3 and ERK/Sp1 signaling pathways

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