CREB activation drives acinar to ductal reprogramming and promote pancreatic cancer progression in animal models of alcoholic chronic pancreatitis.

Background And Aims: induction of alcoholic chronic pancreatitis (ACP) causes significant acinar damage, increased fibroinflammatory response, and heightened activation of cyclic response element binding protein 1 (CREB) when compared with alcohol (A) or chronic pancreatitis (CP) mediated pancreatic damage. However, the study elucidating the cooperative interaction between CREB and the oncogenic (*) in promoting pancreatic cancer progression with ACP remains unexplored.

Methods: Experimental ACP induction was established in multiple mouse models, followed by euthanization of the animals at various time intervals during the recovery periods.

Targeting DNA Repair and Survival Signaling in Diffuse Intrinsic Pontine Gliomas to Prevent Tumor Recurrence.

Therapeutic resistance remains a major obstacle to successful clinical management of diffuse intrinsic pontine glioma (DIPG), a high-grade pediatric tumor of the brain stem. In nearly all patients, available therapies fail to prevent progression. Innovative combinatorial therapies that penetrate the blood-brain barrier and lead to long-term control of tumor growth are desperately needed.

Histone H3 K27M-mediated regulation of cancer cell stemness and differentiation in diffuse midline glioma.

Therapeutic resistance remains a major obstacle to preventing progression of H3K27M-altered Diffuse Midline Glioma (DMG). Resistance is driven in part by ALDH-positive cancer stem cells (CSC), with high ALDH1A3 expression observed in H3K27M-mutant DMG biopsies. We hypothesized that ALDH-mediated stemness and resistance may in part be driven by the oncohistone itself.

N-(2-hydroxyphenyl)-2-phenazinamine from Nocardiopsis exhalans induces p53-mediated intrinsic apoptosis signaling in lung cancer cell lines.

The present study aims to investigate the effect and the molecular mechanism of N-(2-hydroxyphenyl)-2-phenazinamine (NHP) isolated from Nocardiopsis exhalans against the proliferation of human lung cancer cells. The cytotoxic activity of NHP against A549 and H520 cells was determined using MTT assay. The cytotoxic activity of NHP against A549 and H520 lung cancer cells showed excellent activity at 75 μg/mL and damage the mitochondrial membrane and nucleus by generating oxidative stress.

Silencing Sirtuin 6 induces cell cycle arrest and apoptosis in non-small cell lung cancer cell lines.

Sirtuins (SIRT1-7), are NAD-dependent deacetylases and ADP-ribosyl transferases, plays a major part in carcinogenesis. The previous report suggests that in cancer, sirtuins gained tremendous interest and critical regulators of the unusual processes. In carcinogenesis, sirtuins possess either tumor suppressor or promoter.

Annona muricata assisted biogenic synthesis of silver nanoparticles regulates cell cycle arrest in NSCLC cell lines.

With plenteous accessible therapeutics, lung cancer endures a preeminent cause of the worldwide fatality. Apart from medical advancements, various plant parts are still used to treat cancer based on proven tradition. The present study focuses on analysing the anticancer efficacy of silver nanoparticles coupled with the aqueous leaf extract of Annona muricata.

p53 mediated transcriptional regulation of long non-coding RNA by 1-hydroxy-1-norresistomycin triggers intrinsic apoptosis in adenocarcinoma lung cancer.

Over a few decades, systemic chemotherapy and surgery are the only treatment options for lung cancer. Due to limited efficacy and overall poor survival of patients, it is necessary to develop a newer therapeutic strategy which specifically targets cancer cell proliferation pathway. Deciphering the role of long non-coding RNAs (lncRNAs) in tumorigenesis and pathogenesis of cancer cells has recently emerged.

Target delivery of doxorubicin tethered with PVP stabilized gold nanoparticles for effective treatment of lung cancer.

Development of drug delivery system conjugated with doxorubicin (dox) on the surface of AuNPs with polyvinylpyrrolidone (Dox@PVP-AuNPs), we have demonstrated that human lung cancer cells can significantly overcome by the combination of highly effective cellular entry and responsive intracellular release of doxorubicin from Dox@PVP-AuNPs complex. Previously drug release from doxorubicin-conjugated AuNPs was confirmed by the recovered fluorescence of doxorubicin from quenching due to the nanosurface energy transfer between doxorubicinyl groups and AuNPs. Dox@PVP-AuNPs achieved enhanced inhibition of lung cancer cells growth than free Doxorubicin and PVP-AuNPs.

Structural characterization and anticancer activity (MCF7 and MDA-MB-231) of polysaccharides fractionated from brown seaweed Sargassum wightii.

The purpose of this study was to investigate the anticancer activity of polysaccharides from brown seaweed Sargassum wightii (SWP) on human breast cancer cells. Initially, two polysaccharide fractions (SWP1 and SWP2) were isolated and purified from the crude polysaccharides using DEAE-52 cellulose and Sephadex G-100 column chromatography. As a result, SWP1 was obtained with the yield of 21.

Anticancer activity of graphene oxide-reduced graphene oxide-silver nanoparticle composites.

In the present study, a chemical route was employed to synthesize graphene oxide (GO)-reduced graphene oxide (rGO)-Ag nanoparticle (AgNP) composites from graphite and AgNO using vitamin C as reducing agent. Powder X-ray diffraction pattern and field emission scanning electron microscope images revealed that the AgNP were uniformly distributed on the surface of GO and rGO nanosheets. For the first time, the cytotoxicity of GO, rGO, AgNP, GO-AgNP and rGO-AgNP composites were examined against human lung cancer A549 cells using MTT assay and reported quantitatively.

Marine steroid derived from Acropora formosa enhances mitochondrial-mediated apoptosis in non-small cell lung cancer cells.

p53 pathway has been revealed to mediate cellular stress responses and trigger DNA repair, cell cycle arrest, senescence, and apoptosis. We isolated 2-ethoxycarbonyl-2-β-hydroxy-A-nor-cholest-5-ene-4one (ECHC) from butanol extracts of scleractinian coral Acropora formosa and reported its potential antioxidant and antimicrobial activity as well as less toxicity against zebrafish Danio rerio. In the present study, we intend to explore p53-mediated apoptosis pathway enhanced by ECHC in A549 human non-small cell lung cancer cell lines.

Chemopreventive potential of fungal taxol against 7, 12-dimethylbenz[a]anthracene induced mammary gland carcinogenesis in Sprague Dawley rats.

Breast cancer is the second most prevalent cancer and foremost global public health problem. The present study was designed to appraise the chemopreventive potential of fungal taxol against 7,12-dimethylbenz[a]anthracene (DMBA) induced mammary gland carcinogenesis in Sprague Dawley rats. After 90 days of tumor induction, fungal and authentic taxol were given intraperitoneally once in a week for four weeks.

Blocking NF-κB sensitizes non-small cell lung cancer cells to histone deacetylase inhibitor induced extrinsic apoptosis through generation of reactive oxygen species.

NF-κB signalling is one of the main cell survival pathways that attenuate the anticancer efficacy of therapeutic drugs. Previous studies demonstrated that the histone deacetylase (HDAC) inhibitor induces apoptosis in some malignancies through multiple mechanisms including up-regulation of death receptors, disruption of Hsp90 function and generation of reactive oxygen species (ROS). However, HDAC inhibitor also induces a cell survival signal through NF-κB activation.

Romidepsin induces cell cycle arrest, apoptosis, histone hyperacetylation and reduces matrix metalloproteinases 2 and 9 expression in bortezomib sensitized non-small cell lung cancer cells.

Histone deacetylase (HDAC) inhibitors have been proven to be effective therapeutic agents to kill cancer cells through inhibiting HDAC activity or altering the structure of chromatin. We recently reported that chemotherapy by the HDAC inhibitor, romidepsin activates the anti- apoptotic transcription factor NF-κB in A549 non-small cell lung cancer (NSCLC) cells and fails to induce significant levels of apoptosis. We also demonstrated that NF-κB inhibition with proteasome inhibitor bortezomib enhanced HDAC inhibitor induced mitochondrial injury and sensitize A549 NSCLC cells to apoptosis through the generation of reactive oxygen species.