Cytoplasmic p21 Mediates 5-Fluorouracil Resistance by Inhibiting Pro-Apoptotic Chk2.

The oncogenic cytoplasmic p21 contributes to cancer aggressiveness and chemotherapeutic failure. However, the molecular mechanisms remain obscure. Here, we show for the first time that cytoplasmic p21 mediates 5-Fluorouracil (5FU) resistance by shuttling p-Chk2 out of the nucleus to protect the tumor cells from its pro-apoptotic functions.

Zinc suppresses stem cell properties of lung cancer cells through protein kinase C-mediated β-catenin degradation.

Highly tumorigenic cancer stem cells (CSCs) residing in most cancers are responsible for cancer progression and treatment failure. Zinc is an element regulator of several cell functions; however, its role in regulation of stem cell program in lung cancer has not been demonstrated. The present study reveals for the first time that zinc can suppress stem cell properties of lung cancer cells.

Benzophenone-3 increases metastasis potential in lung cancer cells via epithelial to mesenchymal transition.

Exposure to compounds with cancer-potentiating effects can contribute to the progression of cancer. Herein we have discovered for the first time that benzophenone-3 (BP-3), a chemical used as sunscreen in various cosmetic products, enhances the ability of lung cancer cells to undergo metastasis. The exposure of the lung cancer cells to BP-3 at non-toxic concentrations significantly increased the number of anoikis resistant cells in a dose-dependent manner.

Potential Anti-metastasis Natural Compounds for Lung Cancer.

As lung cancer is the most common malignancy worldwide and high mortalities are the result of metastasis, novel information surpassing the treatment strategies and therapeutic agents focusing on cancer dissemination are of interest. Lung cancer metastasis involves increased motility, survival in circulation and ability to form new tumors. Metastatic cells increase their aggressive features by utilizing several mechanisms to overcome hindrances of metastasis, including epithelial to mesenchymal transition (EMT), increased in cellular survival and migratory signals.

Zinc induces epithelial to mesenchymal transition in human lung cancer H460 cells via superoxide anion-dependent mechanism.

Background: Epithelial to mesenchymal transition (EMT) has been shown to be a crucial enhancing mechanism in the process of cancer metastasis, as it increases cancer cell capabilities to migrate, invade and survive in circulating systems. This study aimed to investigate the effect of essential element zinc on EMT characteristics in lung cancer cells.

Methods: The effect of zinc on EMT was evaluated by determining the EMT behaviors using migration, invasion and colony formation assay.

Angiotensin II Increases Cancer Stem Cell-like Phenotype in Lung Cancer Cells.

Background: Cancer stem cells (CSCs) have been proposed as important players in cancer progression, metastasis, and chemotherapeutic resistance in many cancers, including lung cancer. However, effects of the endogenous substance angiotensin II (ANG II) on cancer stem cell-like phenotype in lung cancer are largely unknown.

Materials And Methods: Human lung cancer cells were treated with non-cytotoxic concentrations of ANG II.

Ouabain mediates integrin switch in human lung cancer cells.

Background: Physiological effects of ouabain, an endogenous human hormone, are being intensively investigated. However, its role in regulation of integrin pattern in lung cancer is largely unknown. The switching in the expression pattern of integrins is recognized as an important factor facilitating metastasis of several cancers.

Silymarin selectively protects human renal cells from cisplatin-induced cell death.

Context: Cisplatin-induced nephrotoxicity has been accepted as an important obstacle for efficient cisplatin-based chemotherapy. Silymarin from seeds of milk thistle [Silybum marianum L. (Asteraceae)] has been shown to possess various potential pharmacological properties; however, whether or not this agent selectively protects renal cells from cisplatin-induced cell death with no interfering effect on cancer cells is not clear.