Background Recent evidence demonstrates that the long non-coding RNA (lncRNA) BLACAT1 is associated with the progression and development of various cancers; however, its effect on tumorigenesis of colorectal cancer (CRC) is still poorly understood. The aim of the present study was to investigate the expression and function of BLACAT1 in CRC. Methods Expression data from the GEO and GEPIA databases and results obtained from clinical samples/patients were used to determine the correlation between BLACAT1 expression, and CRC metastasis and overall survival (OS). Furthermore, we knocked down BLACAT1 using short interfering RNA (siRNA) and observed its biological functions using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), cell counting kit-8 (CCK-8) assay, tumor cell clone formation, and Matrigel invasion assays in the HCT116 cell line. Results BLACAT1 level was higher in CRC tissues and cell lines than in normal colon mucosal tissues and cell lines. Correlation of data from the GEO and GEPIA databases with several clinical parameters revealed that CRC patients with high BLACAT1 expression showed poor OS. Multivariate analysis indicated that high BLACAT1 expression is an independent risk factor in patients with CRC. Furthermore, siRNA-mediated knockdown of BLACAT1 suppressed proliferation and invasion of CRC cells in vitro . This in turn was associated with reduced expression of cyclin D1, CDK6, and vimentin, and enhanced expression of E-cadherin. Conclusions BLACAT1 may play an important role in the progression and development of CRC, and may serve as a potential therapeutic target for patients with CRC.

Pancreatic cancer is one of the most aggressive cancers with a median survival time of less than 5 months, and conventional chemotherapeutics are the main treatment strategy. Poly(ADP-ribose) polymerase (PARP) inhibitors have been recently approved for BRCA1/2-mutant pancreatic cancer, opening a new era for targeted therapy for this disease. However, most pancreatic cancer patients carry wild-type BRCA1/2 with resistance to PARP inhibitors. Here, we reported that mammalian target of rapamycin complex 2 (mTORC2) kinase is overexpressed in pancreatic cancer tissues and promotes pancreatic cancer cell growth and invasion. Moreover, we found that knockdown of the mTORC2 obligate subunit Rictor sensitized pancreatic cancer cells to the PARP inhibitor olaparib. Mechanistically, we showed that mTORC2 positively regulates homologous recombination (HR) repair by modulating BRCA1 recruitment to DNA double-strand breaks (DSBs). In addition, we confirmed that combination treatment with the mTORC2 inhibitor PP242 and the PARP inhibitor olaparib synergistically inhibited pancreatic cancer growth in vivo . Thus, this study provides a novel target and strategy for optimizing PARP inhibitor efficiency in pancreatic cancers.

Skin cancer is one of the dangerous form of cancer spreading vigorously among humans, so its early detection is very important for further treatment. Theoretical study on skin tumor detection using long-pulsed infrared thermal wave testing technology (LP-ITWTT) has been carried out. The working principle of LP-ITWTT was described. The 3-D thermal model for skin tumor using LP-ITWTT was established and calculated. The effect of tumor geometry size including radius, depth and thickness to the measurement parameter Cmax is studied, and the influence law has been got, which can provide a theoretical basis for the diagnosis of skin tumors using LP-ITWTT.