Correction: P62 regulates resveratrol-mediated Fas/Cav-1 complex formation and transition from autophagy to apoptosis.

[This corrects the article DOI: 10.18632/oncotarget.2733.

Lasting DNA Damage and Aberrant DNA Repair Gene Expression Profile Are Associated with Post-Chronic Cadmium Exposure in Human Bronchial Epithelial Cells.

Cadmium (Cd) is a widespread environmental pollutant and carcinogen. Although the exact mechanisms of Cd-induced carcinogenesis remain unclear, previous acute/chronic Cd exposure studies have shown that Cd exerts its cytotoxic and carcinogenic effects through multiple mechanisms, including interference with the DNA repair system. However, the effects of post-chronic Cd exposure remain unknown.

DNA methylation of a non-CpG island promoter represses NQO1 expression in rat arsenic-transformed lung epithelial cells.

NAD(P)H:quinone oxidoreductase 1 (NQO1), a phase II flavoenzyme that catalyzes reduction reactions to protect cells against electrophiles and oxidants, is involved in tumorigenesis. Altered methylation of the NQO1 gene has been observed and is speculated to result in aberrant NQO1 expression in rat cells undergoing chemical carcinogenesis, although this has not been proven experimentally. In this study, we first investigated the potential epigenetic mechanisms underlying the phenomenon of NQO1 differential expression in individual subclones of rat arsenic-transformed lung epithelial cells (TLECs).

Resveratrol induces autophagy-dependent apoptosis in HL-60 cells.

Background: All known mechanisms of apoptosis induced by resveratrol act through cell cycle arrest and changes in mitochondrial membrane potential. It is currently unknown whether resveratrol-induced apoptosis is associated with other physiological processes, such as autophagy.

Methods: Apoptosis-related markers involved in the intrinsic and extrinsic apoptotic pathways, and autophagic markers were detected by using western blotting and immunofluorescence.

Aberrant cytokine secretion and zinc uptake in chronic cadmium-exposed lung epithelial cells.

Purpose: Our previous results showed that cadmium (Cd)-adapted lung epithelial cells (LECs) developed resistance to apoptosis due to non-responsiveness of the c-Jun N-terminal kinase pathway and augmented expression of cytokeratin 8. Since cellular Cd entry is a prerequisite in order for Cd to elicit its cytotoxicity, therefore, we wonder if there are differential metal ion transport ability and also other phenotypic changes that occurred in these Cd-resistant LECs.

Experimental Design And Results: Here, we explored further and found that the zinc (Zn) importer Zip8 was stably abolished in these cells along with a marked decrease of Cd and Zn accumulation.

Upregulation of glycolysis and oxidative phosphorylation in benzo[α]pyrene and arsenic-induced rat lung epithelial transformed cells.

Arsenic and benzo[α]pyrene (B[a]P) are common contaminants in developing countries. Many studies have investigated the consequences of arsenic and/or B[a]P-induced cellular transformation, including altered metabolism. In the present study, we show that, in addition to elevated glycolysis, B[a]P/arsenic-induced transformation also stimulates oxidative phosphorylation (OXPHOS).

Proteomics Based Identification of Proteins with Deregulated Expression in B Cell Lymphomas.

Follicular lymphoma and diffuse large B cell lymphomas comprise the main entities of adult B cell malignancies. Although multiple disease driving gene aberrations have been identified by gene expression and genomic studies, only a few studies focused at the protein level. We applied 2 dimensional gel electrophoresis to compare seven GC B cell non Hodgkin lymphoma (NHL) cell lines with a lymphoblastoid cell line (LCL).

Two-dimensional liquid chromatography with tandem mass spectrometry-based proteomic characterization of endometrial luminal epithelial surface proteins responsible for embryo implantation.

Objective: To identify endometrial epithelial cell surface proteins essential for blastocysts implantation.

Design: Isolation of cell-surface labeled prereceptive (pregnancy day 1) and receptive (pregnancy day 4) mouse endometrial proteins coupled to two-dimensional liquid chromatography with tandem mass spectrometry.

Setting: University research laboratory.

P62 regulates resveratrol-mediated Fas/Cav-1 complex formation and transition from autophagy to apoptosis.

Resveratrol is a potential polyphenol drug used in cancer treatment. We examined the relationship between autophagy and apoptosis in RSV-treated non-small lung adenocarcinoma A549 cells. Resveratrol treatment increased autophagy and autophagy-mediated degradation of P62.

Dioscin induced activation of p38 MAPK and JNK via mitochondrial pathway in HL-60 cell line.

Saponins have shown promise in cancer prevention and therapy; however, little is known about the detailed signaling pathways underlying their anticancer activities. In the present study, we examined the mechanisms of action of dioscin, a glucosides saponin isolated from Polygonatum zanlanscianense pump, in human myeloblast leukemia HL-60 cells. Dioscin suppressed HL-60 cell growth in a dose-dependent manner.

Autophagic cell death induced by resveratrol depends on the Ca(2+)/AMPK/mTOR pathway in A549 cells.

Resveratrol has many biological effects, including anti-tumor, antiviral activities, and vascular protection. Recent studies have suggested that resveratrol exert its antitumor effects through induction of autophagy by an unknown mechanism. In this study, we investigated the involvement of autophagy in resveratrol-induced cell death and its potential molecular mechanisms in A549 human lung adnocarcinoma cells.

Resveratrol-induced apoptosis is enhanced by inhibition of autophagy in esophageal squamous cell carcinoma.

The anti-cancer activity of resveratrol in human esophageal squamous cell carcinoma (ESCC) was investigated focusing on the role of autophagy and its effects on apoptotic cell death. We demonstrated that resveratrol inhibits ESCC cell growth in a dose-dependent manner by inducing cell cycle arrest at the sub-G1 phase and resulting in subsequent apoptosis. Mechanistically, resveratrol-induced autophagy in the ESCC cells is AMPK/mTOR pathway independent.

An overview of esophageal squamous cell carcinoma proteomics.

Esophageal squamous cell carcinoma (ESCC) still remains the leading cancer-caused mortality in northern China, in particular in areas nearby Taihang Mountain. Late-stage diagnosis of ESCC increases the mortality and morbidity of ESCC. Therefore, it is imperative to identify biomarkers for early diagnosis, monitoring of tumor progression and identifying potential therapeutic targets of ESCC.

Post-translational modification of human heat shock factors and their functions: a recent update by proteomic approach.

Heat shock factors (HSFs) are vital for modulating stress and heat shock-related gene expression in cells. The activity of HSFs is controlled largely by post-translational modifications (PTMs). For example, basal phosphorylation of HSF1 on three serine sites suppresses the heat shock response, and hyperphosphorylation of HSF1 on several other serine and threonine sites by stress-activated kinases results in its activation, while acetylation on K80 inhibits its DNA-binding ability.

Comparative proteomic analysis of differentiation of mouse F9 embryonic carcinoma cells induced by retinoic acid.

The multipotent mouse F9 embryonic carcinoma cell is an ideal model system to investigate the mechanism of retinoic acid (RA) in cell differentiation and cell growth control and the biochemical basis of early embryonic development. We reported here a proteomics approach to study protein expression changes during the differentiation of F9 cells into the visceral endoderm. F9 cells were incubated with or without RA at 0, 24, 48, and 72 h.

Multiple pathways were involved in tubeimoside-1-induced cytotoxicity of HeLa cells.

The Bolbostemma paniculatum (Maxim.) Franquet (Cucurbitaceae) is a Chinese herb with anticancer potential. Its main active component tubeimoside-1 (TBMS1), a triterpenoid saponin, was previously proved as a potent anticancer chemotherapeutic agent; however, the molecular basis for its activities is still elusive.

Molecular changes during arsenic-induced cell transformation.

Arsenic and its derivatives are naturally occurring metalloid compounds widely distributed in the environment. Arsenics are known to cause cancers of the skin, liver, lung, kidney, and bladder. Although numerous carcinogenic pathways have been proposed, the exact molecular mechanisms remain to be delineated.

Epidermal growth factor-induced epithelial-mesenchymal transition in human esophageal carcinoma cells--a model for the study of metastasis.

Deciphering the molecular basis of esophageal cancer metastasis requires adequate experimental models. Epithelial-mesenchymal transition (EMT) is the hallmark of tumor metastasis. As a promoter of the malignant progression of esophageal cancer, epidermal growth factor (EGF) has been shown to induce EMT in several cell lines.

Biomarkers of lung-related diseases: current knowledge by proteomic approaches.

The lung epithelial surface is one of the vital barriers or sensors in the body responding to the external atmosphere and thereby always subjecting to direct toxicological exposure, stress, stimulus, or infection. Due to its relatively higher sensitivity in response to toxicants, the use of lung epithelial cell culture and lung tissue from animal models or patients has facilitated our learning to lung physiopathology and toxicopharmacology. The recent advancement of proteomics has made it possible to investigate the cellular response at a global level.

Down-regulation of HSP27 sensitizes TRAIL-resistant tumor cell to TRAIL-induced apoptosis.

Tumor necrosis factor-alpha-related apoptosis-inducing ligand (TRAIL) has recently emerged as a cancer therapeutic agent because it preferentially induces apoptosis in human cancer over normal cells. Most tumor cells, including lung cancer cell line A549, unfortunately, are resistant to TRAIL treatment even at high dose. Recent studies indicated that TRAIL-resistant cancer cells could be sensitized to TRAIL by combination therapy.

Identification and characterization of an Nrf2-mediated ARE upstream of the rat glutamate cysteine ligase catalytic subunit gene (GCLC).

The antioxidant response element (ARE) is an essential component of upstream regulatory sequences present on genes for most phase II detoxification enzymes, including the glutamate cysteine ligase catalytic subunit (GCLC). NF-E2-related factor 2 (Nrf2) is a principal transcription factor that binds to the ARE and plays a key role in cellular responses to stress via the Keap1-Nrf2-ARE pathway. However, the ARE that mediates human GCLC gene expression has not been found in the rat.

Tubeimoside-1 exerts cytotoxicity in HeLa cells through mitochondrial dysfunction and endoplasmic reticulum stress pathways.

Traditional Chinese herbal medicines are a great source of cancer chemotherapeutic agents. Tubeimoside-1 (TBMS1) is a triterpenoid saponin extracted from Bolbostemma paniculatum (Maxim.) Franquet (Cucurbitaceae), a Chinese herb with anticancer potential named as "Tu Bei Mu".

Mammary serine protease inhibitor inhibits epithelial growth factor-induced epithelial-mesenchymal transition of esophageal carcinoma cells.

Background: By using proteomic technology, the authors previously observed the substantial down-regulation of mammary serine protease inhibitor (maspin) in esophageal squamous cell carcinoma and metastases. In the current study, they examined the effects of maspin re-expression in a maspin-null esophageal cancer cell line EC109 and also investigated the underlying mechanism.

Methods: A cell line with stable maspin expression was established.

Proteomic identification of tumor-associated protein in ovarian serous cystadenocarinoma.

Ovarian epithelial serous cystadenocarcinoma (OESC) is the most lethal of all gynecologic malignancies. In this report, we performed comparative proteomic study of normal ovarian epithelial and OESC tissue in order to establish OESC related protein atlas, and to identify tumor-associated proteins which may be important target proteins for clinical diagnosis and therapy and/or closely correlated to OESC pathogenesis. Six proteins were found significantly differentially expressed between normal ovarian epithelial and OESC tissues.