English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Particularly interesting new cysteine-histidine rich protein (PINCH) is related to poor outcome in colorectal cancers. Here, the relationship between PINCH-1 and cell survival in colon cancer cells was analyzed and the signaling pathways regulated by PINCH-1 by using PINCH-1 siRNA. KM12C cells were treated with PINCH-1 siRNA or control siRNA. Cell number was analyzed by crystal violet staining and caspase-3 activity was assessed using a fluorescent substrate. PINCH-1 extra- and intracellular pathways in KM12C cells were investigated, using phospho-kinase/phospho-receptor tyrosine kinase (RTK) antibody arrays. The expression of c-Myc was evaluated by Quantitative real-time PCR (qPCR) and Western blot analysis. Cell number was significantly decreased ( P =0.003) and the caspase-3 activity increased ( P =0.019) in PINCH-1 depleted KM12C cultures compared to siRNA cultures. In PINCH-1 silenced KM12C cells, the levels of EGFR and ERK1/2 were significantly decreased ( P =0.008, P= 0.003, respectively) compared to their controls, as were the c-Myc mRNA and protein expressions ( P =0.0073, P= 0.0002, respectively). Down-regulation of PINCH-1 reduced the cell survival and lowers the levels of EGFR, ERK1/2 and c-Myc in colon cancer cells. PINCH-1 is essential for cell survival, and may be a future target for anticancer therapy.

Down-regulation of PINCH-1 Reduces Expression of EGFR, ERK1/2 and c-Myc, and Leads to Loss of Cell Viability in Colon Cancer Cells