Fluid shear stress induces epithelial-mesenchymal transition (EMT) in Hep-2 cells

Abstract

Laryngeal squamous cell carcinoma (LSCC) is one of the most commonly diagnosed malignancies with high occurrence of tumor metastasis, which usually exposes to fluid shear stress (FSS) in lymphatic channel and blood vessel. Epithelial-mesenchymal transition (EMT) is an important mechanism that induces metastasis and invasion of tumors. We hypothesized that FSS induced a progression of EMT in laryngeal squamous carcinoma. Accordingly, the Hep-2 cells were exposed to 1.4 dyn/cm2 FSS for different durations. Our results showed that most of cells changed their morphology from polygon to elongated spindle with well-organized F-actin and abundant lamellipodia/filopodia in protrusions. After removing the FSS, cells gradually recovered their flat polygon morphology. FSS induced Hep-2 cells to enhance their migration capacity in a time-dependent manner. In addition, FSS down-regulated E-cadherin, and simultaneously up-regulated N-cadherin, translocated β-catenin into the nucleus. These results confirmed that FSS induced the EMT in Hep-2 cells, and revealed a reversible mesenchymal-epithelial transition (MET) process when FSS was removed. We further examined the time-expressions of signaling cascades, and demonstrated that FSS induces the EMT and enhances cell migration depending on integrin-ILK/PI3K-AKT-Snail signaling events. The current study suggests that FSS, an important biophysical factor in tumor microenvironment, is a potential determinant of cell behavior and function regulation.

Fluid shear stress induces cell migration and invasion via activating autophagy in HepG2 cells

“…Qazi et al found that FSS at 0.84 and 2.53 dyn/cm 2 enhanced the metastatic potential of metastatic cell [10,11]. We previously demonstrated that FSS induced the changes in cell morphology and migration capacity of cancer cells including laryngeal squamous cell carcinoma Hep-2 cells and HCC HepG2 cells [12,13]. FSS at 1.4 dyn/cm 2 induced the epithelial-mesenchymal transition of Hep-2 cells through integrin-ILK/PI3K-AKT-Snail signaling pathway [12], which might contribute to cancer metastasis [14,15].…”

Protective Effects of Hydrogen Sulfide Against Cigarette Smoke Exposure-Induced Placental Oxidative Damage by Alleviating Redox Imbalance via Nrf2 Pathway in Rats

“…The Western blot analysis was performed as previous study described [51]. Briefly, the placental tissue was homogenized independently in RIPA buffer (Beyotime, Nanjing, Jiangsu, China) with 1% phenylmethylsulfonyl fluoride (Beyotime, Nanjing, Jiangsu, China) and protease inhibitor (Sigma Aldrich, St Louis, MO, USA) according to the manufacturer's instructions at 4°C.…”

Nuclear nonmetastatic protein 23‐H1 expression and epithelial‐mesenchymal transition in laryngeal carcinoma: A pilot investigation

“…Most of the studies on epithelial-to-mesenchymal transition in laryngeal SCC have been intriguing investigations based on cancer cell lines, [18][19][20][21][22][23][24] whereas few studies have considered the clinicopathological and prognostic role of epithelial-tomesenchymal transition in laryngeal SCC. Using immunohistochemistry, Goulioumis et al 25 transition in 80 human laryngeal SCCs, finding that estrogen receptor-ß expression correlated positively with the maintenance of E-cadherin and ß-catenin at cell junctions, and negatively with the loss of E-cadherin, the nuclear translocation of ß-catenin, and a higher TNM classification.…”