Attenuation of cisplatin-induced acute kidney injury by N-(2-Hydroxyphenyl) acetamide and its gold conjugated nano-formulations in mice.

The attenuation of cisplatin-induced acute kidney injury (AKI) in mice by N-(2-hydroxyphenyl) acetamide (NA-2) and NA-2-conjugated gold nanoparticles (NA2-AuNPs) was investigated. Male BALB/c mice (n = 54) were divided into nine groups having six animals in each group. Animals in groups 3-9 were pre-treated for 5 days with test compounds, whereas, animals in group 1 and 2 received normal saline. On day 4, animals in groups 2, 3, 4, 5, 6 and 9 were given single intra-peritoneal injection of CP at the dose of 5 mg/kg. After 72 hours of CP injection, all animals were sacrificed. Blood was collected for serum urea and creatinine estimation, and kidneys were harvested for histo-pathological examinations and qPCR studies for nuclear factor-κB p50, (NFκB) ; inducible nitric oxide synthase (iNOS); hemeoxygenase-1 (HO-1); and interleukin-6 (IL-6).NA-2 and NA2-AuNPs was observed to decrease the serum urea and creatinine levels. Both the test compounds reduced kidney injury damage score and improved histological architecture in the treated animals in dose dependent manner. Furthermore, the mRNA expressions of NFkB p50, iNOS and IL-6 genes were down-regulated, and HO-1 gene was up-regulated in the animals treated with the test compounds. It is concluded that NA-2 and NA2-AuNPs attenuates CP-induced AKI in mice models through anti-inflammatory and anti-oxidant mechanisms.

Cancer Cell-derived Secretory Factors in Breast Cancer-associated Lung Metastasis: Their Mechanism and Future Prospects.

In Breast cancer, Lung is the second most common site of metastasis after the bone. Various factors are responsible for Lung metastasis occurring secondary to Breast cancer. Cancer cellderived secretory factors are commonly known as 'Cancer Secretomes'. They exhibit a prompt role in the mechanism of Breast cancer lung metastasis. They are also major constituents of hostassociated tumor microenvironment. Through cross-talk between cancer cells and the extracellular matrix components, cancer cell-derived extracellular matrix components (CCECs) such as hyaluronan, collagens, laminin and fibronectin cause ECM remodeling at the primary site (breast) of cancer. However, at the secondary site (lung), tenascin C, periostin and lysyl oxidase, along with pro-metastatic molecules Coco and GALNT14, contribute to the formation of pre-metastatic niche (PMN) by promoting ECM remodeling and lung metastatic cells colonization. Cancer cell-derived secretory factors by inducing cancer cell proliferation at the primary site, their invasion through the tissues and vessels and early colonization of metastatic cells in the PMN, potentiate the mechanism of Lung metastasis in Breast cancer. On the basis of biochemical structure, these secretory factors are broadly classified into proteins and non-proteins. This is the first review that has highlighted the role of cancer cell-derived secretory factors in Breast cancer Lung metastasis (BCLM). It also enumerates various researches that have been conducted to date in breast cancer cell lines and animal models that depict the prompt role of various types of cancer cell-derived secretory factors involved in the process of Breast cancer lung metastasis. In the future, by therapeutically targeting these cancer driven molecules, this specific type of organ-tropic metastasis in breast cancer can be successfully treated.