PTSA-induced synthesis, and nano study of novel ethylquinolin-thiazolo-triazole in cervical cancer.

p-Toluenesulfonic acid-(PTSA) and grinding-induced novel synthesis of ethylquinolin-thiazolo-triazole derivatives was performed using green chemistry. Development of a nanoconjugate drug-delivery system of ethylquinolin-thiazolo-triazole was carried out with D-α-tocopheryl polyethylene glycol succinate (TPGS) and the formulation was further characterized by transmission electron microscopy, atomic force microscopy, dynamic light scattering and drug release assay. The effect of nanoparticles was assessed against a cervical cancer cell line (HeLa) through the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and the effect on apoptosis was determined.

Novel pyrimido-pyridazine derivatives: design, synthesis, anticancer evaluation and studies.

A novel pyrimido-pyridazine derivative for developing anticancer agents was synthesized via Ullmann arylation using an efficient Cu(OAc) catalyst. Compounds were investigated for their anticancer potential, against human breast adenocarcinoma cells, viz. MCF-7, MDA-MB-231 and normal cell line HEK-293.

Sodium sulphide promoted synthesis of fused quinoline at room temperature.

A novel, simple and eco-friendly strategy for the synthesis of thiopyrano[4,3-]quinolin-1-ones and pyrrolo[3,4-]quinolin-1-ones from 2-alkynylquinoline-3-carbonitriles and sodium sulphide (NaS·9HO) under catalyst-free conditions at room temperature has been described. In this reaction, a readily available inorganic salt (NaS·9HO) serves as the sulphur source and leads to the generation of diverse functionalized thiopyrano[4,3-]quinolin-1-ones and pyrrolo[3,4-]quinolin-1-ones in moderate to excellent yields through sulfuration, annulation, and aerial oxidation.

Cancer stem cell generation during epithelial-mesenchymal transition is temporally gated by intrinsic circadian clocks.

Epithelial-mesenchymal transition (EMT) is a key event preceding tumor cell metastasis that increases cell invasiveness and cancer stem cell (CSC) populations. Studies suggest that genes used in generating circadian rhythms also serve in regulating EMT. To test the role of circadian clocks in cellular EMT events two cancer cell lines were compared, one that has a well-established circadian clock, C6 from rat glioma, and one that does not, MCF-7 from human breast tumor.

The hepatokine Tsukushi gates energy expenditure via brown fat sympathetic innervation.

Thermogenesis is an important contributor to whole body energy expenditure and metabolic homeostasis. Although circulating factors that promote energy expenditure are known, endocrine molecules that suppress energy expenditure have remained largely elusive. Here we show that Tsukushi (TSK) is a liver-enriched secreted factor that is highly inducible in response to increased energy expenditure.

The circadian clock modulates anti-cancer properties of curcumin.

Background: Curcuminoids of the spice turmeric and their enhanced derivatives have much potential as cancer treatments. They act on a wide variety of biological pathways, including those regulating cell division and circadian rhythms. It is known that circadian clocks can modify cancer therapy effectiveness, according to studies aimed at optimizing treatments based on the circadian cycle.

Circadian properties of cancer stem cells in glioma cell cultures and tumorspheres.

Increased cancer risk is linked to disruption of circadian rhythms. Cancer stem cells (CSCs) are a known cause of cancer aggressiveness, but their circadian properties have not been described. We discovered circadian rhythms in gene expression within C6 glioma tumorspheres enriched in CSCs and found that the circadian clock is particularly robust in medium lacking any growth factors.

Major differences between tumor and normal human cell fates after exposure to chemotherapeutic monofunctional alkylator.

The major dilemma of cancer chemotherapy has always been a double-edged sword, producing resistance in tumor cells and life-threatening destruction of nontumorigenic tissue. Glioblastoma is the most common form of primary brain tumor, with median survival at 14 months after surgery, radiation and temozolomide (monofunctional alkylator) therapy. Treatment failure is most often due to temozolomide-resistant tumor growth.

Prolonged cell cycle response of HeLa cells to low-level alkylation exposure.

Alkylation chemotherapy has been a long-standing treatment protocol for human neoplasia. N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) is a direct-acting monofunctional alkylator. Temozolomide is a clinical chemotherapeutic equivalent requiring metabolic breakdown to the alkylating agent.