Naphtho[b]-fused BODIPYs have been facilely synthesized via Suzuki-Miyaura-Knoevenagel reaction between mono-iodo-BODIPY or 2,6-diiodo-BODIPY with (2-formylphenyl)boronic acid. This one-pot reaction represents a very straightforward approach for tuning the absorption and emission of BODIPYs in the red visible/NIR range.

IntroductionAntidifferentiation noncoding RNA (ANCR) is a newly identified long noncoding RNA, which is reported to function as an oncogene in multiple human cancers. However, its function in nasopharyngeal carcinoma (NPC) and underlying mechanism are still unclear.Materials and methodsWe explored the expression of ANCR in NPC tissues and cells by real-time PCR and analyzed the relationship between ANCR expression and clinicopathological characteristics of NPC patients by Pearson’s chi-squared test. Then we inhibited ANCR expression in NPC cells using siRNAs and evaluated the effect of ANCR expression on cell proliferation, colony formation, and radiosensitivity by cell counting kit-8 assay and colony formation assay. We used RT-PCR and Western blot analyses to search target genes of ANCR. Also, we used RNA immunoprecipitation (RIP) assay and chromatin immunoprecipitation assay to study the molecular mechanism in this regulation.ResultsWe found that ANCR was upregulated in NPC tissues and cells. ANCR expression was significantly correlated with tumor size and TNM stage. Further, ANCR knockdown inhibited NPC cell growth and radiation resistance. Mechanistically, we found that PTEN was upregulated in ANCR knockdown NPC cells. In addition, RIP assay indicated that EZH2, the oncogenic histone methyltransferase of polycomb repressive complex 2, interacted with ANCR in NPC cells. More importantly, the binding of EZH2 and deposition of relevant negative histone marker H3K27me3 on PTEN promoter depended on ANCR expression.ConclusionANCR expression is upregulated in NPC and promotes NPC growth and radiation resistance through an epigenetic regulation of PTEN expression.

Long noncoding RNAs (lncRNAs) are associated with the development, progression, and prognosis of human cancers. However, the clinical significance and biological function of lncRNAs in hypopharyngeal squamous cell carcinoma (HSCC) remain largely unknown. We characterized the novel lncRNA AB209630 in vivo and in vitro. First, using qRT-PCR, we evaluated whether AB209630 levels differ between HSCC tissues/cell lines and adjacent normal tissues/cell lines. We then assessed whether AB209630 expression levels stimulate or inhibit proliferation, invasion, apoptosis, and metastasis in vitro. Finally, we investigated whether AB209630 levels in tumor tissues were associated with survival outcomes. Our results demonstrated that AB209630 levels were markedly lower in HSCC tissues and cells than in normal tissues and cells, and increased expression of AB209630 level significantly inhibited growth, metastasis, and invasion and stimulated apoptosis in vitro. In addition, patients with decreased expression of AB209630 had a significantly poorer prognosis than those with high AB209630 expression. These data suggest that increased expression of AB209630 might either stimulate or inhibit biological activities involved in HSCC development, indicating a potential application of AB209630 in future treatment for this disease. This study suggest that AB209630 functions as a tumor suppressor in HSCC, and its decreased expression may help predict a poor prognostic outcome of HSCC. Our future work will focus on the mechanisms of whether and how AB209630 as a tumor suppressor gene is involved in HSCC development.

The PHLPP (pleckstrin homology [PH] domain leucine rich repeat protein phosphatase) family, which represents a family of novel Ser/Thr protein phosphatases, is composed of 2 members: PHLPP1 and PHLPP2. PHLPPs partake in diverse cellular activities to exhibit their antitumor and metastasis suppressor functions. It is necessary to investigate the expression patterns of PHLPP1 and PHLPP2 in hypopharyngeal squamous cell carcinomas (HSCCs) and clarify their clinical significance. A total of 138 patients with primary HSCC who underwent curative surgical treatment as an initial treatment were enrolled in this study. A total of 138 HSCC specimens and 64 adjacent noncancerous mucosal epithelial tissues were collected. The expression levels of PHLPP1 and PHLPP2 were examined by quantitative reverse transcription polymerase chain reaction and immunohistochemistry assays. Correlations between clinicopathological parameters of the patients were further evaluated. PHLPP1 and PHLPP2 mRNA transcript levels were significantly lower in tumor samples than in paired adjacent nontumor mucosae (P<0.0001, both). Positive correlations were observed between the mRNA levels of PHLPP1 and PHLPP2 in HSCC tissues (correlation coefficient r = 0.678, P<0.001) and in adjacent nontumor mucosae (r = 0.460, P<0.001). The majority of the noncancerous tissues showed high expression levels of PHLPP1 (87.5%, 56/64) and PHLPP2 (85.9%, 55/64). However, the expressions of PHLPP1 and PHLPP2 were significantly decreased in 83.3% (115/138) and 82.6% (114/138) of tumor tissues, respectively (P<0.0001, both). The expressions of both PHLPP isoforms were significantly related to the tumor clinical stage, differentiation, and cervical lymph node metastasis (P<0.05, all). It was PHLPP1 but not PHLPP2 that was significantly related to the tumor T stage. Low PHLPP1 and PHLPP2 expressions were associated with poor overall survival (OS) in HSCC patients (P = 0.004, P = 0.008, respectively). Multivariate analysis revealed that PHLPP1 was an independent prognostic factor for OS. This study indicates that, in HSCC, aberrant expressions of PHLPP1 and PHLPP2 are common events, and loss of PHLPPs might identify patients with poor prognostic outcomes.