S100A11 is a potential prognostic marker for clear cell renal cell carcinoma

Gabril, Manal; Girgis, Hala; Scorilas, Andreas; Rotondo, Fabio; Wala, Samantha Jane; Bjarnason, Georg A.; Ding, Qiang; Evans, Andrew; Tawedrous, Eriny; Finelli, Antonio; Al-Haddad, Sahar; Yousef, George M.

doi:10.1007/s10585-015-9758-6

Cited by 16 publications

(13 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The binding of Ca 2+ triggers conformational changes of S100A11, which facilitates its interaction with target proteins. S100A11 has been reported to be overexpressed in numerous different types of human cancer, including renal cell carcinoma, lung adenocarcinoma and papillary thyroid carcinoma ( 23 – 26 ). Our previous study revealed that S100A11 serves an important role in the development and prognosis of pancreatic cancer ( 15 ).…”

Section: Discussionmentioning

confidence: 99%

S100A11 promotes human pancreatic cancer PANC‑1 cell proliferation and is involved in the PI3K/AKT signaling pathway

Xiao

et al. 2017

Oncol Lett

View full text Add to dashboard Cite

S100A11, a member of S100 calcium-binding protein family, is associated with the numerous processes of tumorigenesis and metastasis. In the present study, the role of S100A11, and its possible underlying mechanisms in cell proliferation, apoptosis and cell cycle distribution in human pancreatic cancer were explored. Immunohistochemical analyses of S100A11 and phosphorylated (p)-AKT serine/threonine kinase (AKT) were performed in 30 resected specimens from patients with pancreatic cancer. PANC-1 cells were transfected with pcDNA3.1-S100A11 or treated with 50 µmol/l LY294002 for 48 h. Cell proliferation was determined using a cell counting kit-8 assay, whereas apoptosis and cell cycle distribution were determined by flow cytometry analysis. The mRNA and protein levels of S100A11, and AKT were determined using semi quantitative reverse transcription-polymerase chain reaction and western blot analyses, respectively. Pearson correlation analysis revealed that the expression levels of S100A11 and p-AKT were positively correlated (r, 0.802; P<0.05). Compared with the control group, S100A11 overexpression significantly promoted PANC-1 cell proliferation and reduced the percentage of early apoptotic cells. Flow cytometric analysis indicated that the proportion of PANC-1 cells in the S phase was significantly elevated and cell percentage in the G0/G1 phase declined in response to S100A11 overexpression (all P<0.05). S100A11 overexpression also significantly increased AKT mRNA and p-AKT protein expression levels (both P<0.05). The phosphoinositide 3-kinase (PI3K) inhibitor, LY294002, significantly inhibited PANC-1 cell proliferation, promoted apoptosis and caused G1/S phase arrest in PANC-1 cells (all P<0.05). These findings together suggest that S100A11 promotes the viability and proliferation of human pancreatic cancer PANC-1 cells through the upregulation of the PI3K/AKT signaling pathway. Thus, S100A11 may be considered as a novel drug target for targeted therapy of pancreatic cancer.

show abstract

Section: Discussionmentioning

confidence: 99%

S100A11 promotes human pancreatic cancer PANC‑1 cell proliferation and is involved in the PI3K/AKT signaling pathway

Xiao

et al. 2017

Oncol Lett

View full text Add to dashboard Cite

show abstract

“…The downregulated genes included S100A11, which is highly related to cellular motility in cancer. [19][20][21][22][23] It is overexpressed in a large variety of invasive carcinomas, and its suppression substantially decreases cell migration. 21,23 Therefore, the reduced motility of siBC200-transfected HeLa cells could result from the BC200 RNA-knockdown-induced downregulation of S100A11.…”

Section: Depletion Of Bc200 Rna Disrupts the Migration And Invasion Omentioning

confidence: 99%

“…Since BC200 RNA is highly expressed in some breast cancer cells [19][20][21][22][23] we also analyzed the connection between BC200 RNA, cell motility, and S100A11 expression (Fig 9). We found that the BC200 RNA knockdown decreased the wound-healing rate.…”

Section: Bc200 Rna Knockdown Decreases Cell Motility and S100a11 Exprmentioning

confidence: 99%

“…[19][20][21][22][23] This calciumbinding protein is known to promote cellular motility by maintaining outer membrane integrity. [19][20][21][22][23] Ribosome profiling showed reducing expression of S100A11 following BC200 knockdown. Further analysis revealed that S100A11 was reduced at both the mRNA and protein levels following BC200 RNA knockdown, suggesting that the reduced footprints mainly resulted from the downregulation of mRNA.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Knockdown of BC200 RNA expression reduces cell migration and invasion by destabilizing mRNA for calcium-binding protein S100A11

et al. 2017

View full text Add to dashboard Cite

Although BC200 RNA is best known as a neuron-specific non-coding RNA, it is overexpressed in various cancer cells. BC200 RNA was recently shown to contribute to metastasis in several cancer cell lines, but the underlying mechanism was not understood in detail. To examine this mechanism, we knocked down BC200 RNA in cancer cells, which overexpress the RNA, and examined cell motility, profiling of ribosome footprints, and the correlation between cell motility changes and genes exhibiting altered ribosome profiles. We found that BC200 RNA knockdown reduced cell migration and invasion, suggesting that BC200 RNA promotes cell motility. Our ribosome profiling analysis identified 29 genes whose ribosomal occupations were altered more than 2-fold by BC200 RNA knockdown. Many (> 30%) of them were directly or indirectly related to cancer progression. Among them, we focused on S100A11 (which showed a reduced ribosome footprint) because its expression was previously shown to increase cellular motility. S100A11 was decreased at both the mRNA and protein levels following knockdown of BC200 RNA. An actinomycin-chase experiment showed that BC200 RNA knockdown significantly decreased the stability of the S100A11 mRNA without changing its transcription rate, suggesting that the downregulation of S100A11 was mainly caused by destabilization of its mRNA. Finally, we showed that the BC200 RNAknockdown-induced decrease in cell motility was mainly mediated by S100A11. Together, our results show that BC200 RNA promotes cell motility by stabilizing S100A11 transcripts.

show abstract

“…; each category has a score from 1 to 3, and then both scores are added together). 38,39 End-stage (n = 3)…”

Section: Ihc Scoring Quantitative Image Analysis and Statistical Anmentioning

confidence: 99%

Integrated Molecular Analysis of Papillary Renal Cell Carcinoma and Precursor Lesions Unfolds Evolutionary Process from Kidney Progenitor-Like Cells

Saleeb

Farag

Ding

et al. 2019

The American Journal of Pathology

Self Cite

View full text Add to dashboard Cite

Papillary renal cell carcinoma (PRCC) is the most common type of RCC in end-stage kidney disease (ESKD). Papillary adenoma (PA) is a small benign lesion morphologically similar to PRCC and is suggested to be its precursor. PA is also prevalent in ESKD. The evolution of PAs to PRCCs and their relationship to ESKD are poorly understood. A total of 140 PAs, normal kidneys, ESKDs, and PRCCs were analyzed. Previously described markers of renal tubular progenitor cells were analyzed using immunohistochemistry and quantified with digital analysis. Progenitor cells were significantly increased in ESKD (P < 0.0001) and PAs (P Z 0.02) in comparison with the normal kidney. Pathway analysis using global miRNA and chromosomal copy number variations revealed a common developmental theme between PA and the PRCCs. Whole exome sequencing showed a KMT2C-specific pathogenic mutation among all PAs and PRCCs. KMT2C is a chromosome 7 epigenetic regulator implicated in development and oncogenesis. Collectively, results show possible connection of PRCCs to PA and the progenitor-like cell population, which are increased in response to renal tubular injury. In addition, each PRCC histologic subtype had its own set of mutational changes, indicating divergence from a common precursor. The study reports previously unknown biological aspects of PRCC development and could influence current surveillance criteria and early detection strategies of PRCC tumors.

show abstract

S100A11 is a potential prognostic marker for clear cell renal cell carcinoma

Cited by 16 publications

References 31 publications

S100A11 promotes human pancreatic cancer PANC‑1 cell proliferation and is involved in the PI3K/AKT signaling pathway

S100A11 promotes human pancreatic cancer PANC‑1 cell proliferation and is involved in the PI3K/AKT signaling pathway

Knockdown of BC200 RNA expression reduces cell migration and invasion by destabilizing mRNA for calcium-binding protein S100A11

Integrated Molecular Analysis of Papillary Renal Cell Carcinoma and Precursor Lesions Unfolds Evolutionary Process from Kidney Progenitor-Like Cells

Contact Info

Product

Resources

About