Laparoscopic hepatectomy may be a better option for patients with small HCC located on the liver surface and left lateral lobe. The short-term outcome of MWA is promising, although the high risk of local recurrence after the operation should be considered when planning treatment.

A novel doxorubicin (DOX) prodrug (MPEG-b-DOX) was synthesized that reduces the proportion of inactive materials and minimizes drug leak.

Chemotherapy resistance is one of the major challenges for the treatment of osteosarcoma ( OS ). The potential roles of oestrogenic signals in the chemoresistance of OS cells were investigated. As compare to the parental cells, the doxorubicin and cisplatin ( CDDP ) resistant OS cells had greater levels of oestrogen‐related receptors alpha ( ERR α). Targeted inhibition of ERR α by its specific si RNA s or inverse agonist XCT ‐790 can restore the sensitivity of OS resistant cells to chemotherapy. This might be due to that si‐ ERR α can decrease the expression of P‐glycoprotein (P‐gp, encoded by ABCB 1), one important ABC membrane transporter for drug efflux. XCT ‐790 can decrease the transcription and mRNA stability of ABCB 1, while had no effect on protein stability of P‐gp. ERR α can bind to the transcription factor of SP 3 to increase the transcription of ABCB 1. Furthermore, XCT ‐790 treatment decreased the expression of miR‐9, which can bind to the 3′ UTR of ABCB 1 and trigger its decay. Collectively, we found that ERR α can regulate the chemoresistance of OS cells via regulating the transcription and mRNA stability of ABCB 1. Targeted inhibition of ERR α might be a potential approach for OS therapy.

Hepatocellular carcinoma (HCC) is one of the most common causes of cancer-related death worldwide. In the present study, we aimed to profile the possible changes in plasma phospholipid fatty acid composition of HCC patients, and to identify the fatty acid biomarkers that could distinguish HCC patients from healthy controls. A total of 37 plasma samples from healthy controls and HCC patients were collected and their phospholipid fatty acid profiles were characterized by gas chromatography-mass spectrometry followed by multivariate statistical analysis. Twenty-five fatty acids were identified and quantified, their proportions varied greatly between two groups, suggesting each group has its own fatty acid pattern. Orthogonal partial least squares discriminant analysis in terms of fatty acid profiles showed that HCC patients could be clearly distinguished from healthy controls. More importantly, linoleic acid (18:2n-6), oleic acid (18:1n-9), arachidonic acid (20:4n-6) and palmitic acid (16:0) were identified as the potential fatty acid biomarkers of HCC patients. Additionally, to further identify the major cause of the abnormality of plasma fatty acid profile, fatty acid distributions of cancerous tissue and its surrounding tissue from 42 HCC patients were also examined. Due to have similar variation trend of major fatty acid biomarkers, linoleic acid (18:2n-6), oleic acid (18:1n-9), abnormalities in plasma phospholipid fatty acid profiles of HCC patients may be mainly attributed to the alternation of intrinsic fatty acid metabolism caused by cancer per se, but not to the differences in dietary factors.

Long non‐coding RNAs (lncRNAs) have been indicated for the regulatory roles in cardiovascular diseases. This study determined the expression of lncRNA TNK2 antisense RNA 1 (TNK2‐AS1) in oxidized low‐density lipoprotein (ox‐LDL)‐stimulated human aortic smooth muscle cells (HASMCs) and examined the mechanistic role of TNK2‐AS1 in the proliferation and migration of HASMCs. Our results demonstrated that ox‐LDL promoted HASMC proliferation and migration, and the enhanced proliferation and migration in ox‐LDL‐treated HASMCs were accompanied by the up‐regulation of TNK2‐AS1. In vitro functional studies showed that TNK2‐AS1 knockdown suppressed cell proliferation and migration of ox‐LDL‐stimulated HASMCs, while TNK2‐AS1 overexpression enhanced HASMC proliferation and migration. Additionally, TNK2‐AS1 inversely regulated miR‐150‐5p expression via acting as a competing endogenous RNA (ceRNA), and the enhanced effects of TNK2‐AS1 overexpression on HASMC proliferation and migration were attenuated by miR‐150‐5p overexpression. Moreover, miR‐150‐5p could target the 3’ untranslated regions of vascular endothelial growth factor A (VEGFA) and fibroblast growth factor 1 (FGF1) to regulate FGF1 and VEGFA expression in HASMCs, and the inhibitory effects of miR‐150‐5p overexpression in ox‐LDL‐stimulated HASMCs were attenuated by enforced expression of VEGFA and FGF1. Enforced expression of VEGFA and FGF1 also partially restored the suppressed cell proliferation and migration induced by TNK2‐AS1 knockdown in ox‐LDL‐stimulated HASMCs, while the enhanced effects of TNK2‐AS1 overexpression on HASMC proliferation and migration were attenuated by the knockdown of VEGFA and FGF1. Collectively, our findings showed that TNK2‐AS1 exerted its action in ox‐LDL‐stimulated HASMCs via regulating VEGFA and FGF1 expression by acting as a ceRNA for miR‐150‐5p.

A surface molecular imprinting polymer (SMIP) with doxorubicin (DOX) as the template was prepared on the surface of mesoporous silica nanoparticles (MSNs), which were further used as DOX carriers. The loading amount of DOX was calculated as 10.5±0.2 wt% with loading efficiency of 70±8%. The DOX release was controlled because the monomer molecule used in polymerization of SMIP containing sulfur-sulfur bonding, which could be decomposed with an acidic pH and glutathione (GSH). Under an acidic pH and high concentration of GSH, there was greater release of DOX than under normal physiological conditions, which induced less damage to normal cells than to cancer cells. Confocal laser scanning microscopy studies verified the invasion of the DOX within SMIP into TCA8113 cancer cells. These results indicate that the prepared SMIP was an effective nanocarrier.

No abstract

In recent years, the deoxycytidine analogue gemcitabine (2′,2′,-difluorodeoxycytidine) has become the first-line chemotherapeutic agent for patients with pancreatic cancer. However, due to the intrinsic resistance of pancreatic cancer cells, gemcitabine-based chemotherapy yields limited disease control, with >85% disease progression at 6 months from diagnosis. Therefore, elucidating the mechanisms of chemoresistance is a critical step in improving cancer therapy, especially for the treatment of pancreatic cancer. We show PROM2, a transmembrane glycoprotein, is ubiquitously upregulated in pancreatic cancer cell. We also found higher PROM2 expression is associated with shortened overall and disease-free survival times in patients diagnosed with pancreatic cancer. We provide evidence that PROM2 promotes chemoresistance to gemcitabine both in vivo and in vitro. Mechanistically, we demonstrate that PROM2 could directly interacted with Akt and activates the Akt signaling pathway, which thus inhibiting gemcitabineinduced apoptosis. As further evidence, we show PROM2 expression and Akt phosphorylation both promote gemcitabine chemoresistance, and cause poorer survival in clinical samples with pancreatic cancer. Combining gemcitabine with the Akt inhibitor MK-2206 facilitated significant tumor shrinkage and dramatically elevated the survival status in mice xenografted with pancreatic cancer cells. Our findings not only establish PROM2 as a novel positive regulator of the Akt signaling pathway and a candidate prognostic indicator of gemcitabine response, but also provide a neo-therapeutic approach for patients resistant to gemcitabine treatment.