High-Sensitivity 2D MoS2/1D MWCNT Hybrid Dimensional Heterostructure Photodetector.

A photodetector based on a hybrid dimensional heterostructure of laterally aligned multiwall carbon nanotubes (MWCNTs) and multilayered MoS2 was prepared using the micro-nano fixed-point transfer technique. Thanks to the high mobility of carbon nanotubes and the efficient interband absorption of MoS2, broadband detection from visible to near-infrared (520-1060 nm) was achieved. The test results demonstrate that the MWCNT-MoS2 heterostructure-based photodetector device exhibits an exceptional responsivity, detectivity, and external quantum efficiency. Specifically, the device demonstrated a responsivity of 3.67 × 103 A/W (λ = 520 nm, Vds = 1 V) and 718 A/W (λ = 1060 nm, Vds = 1 V). Moreover, the detectivity (D*) of the device was found to be 1.2 × 1010 Jones (λ = 520 nm) and 1.5 × 109 Jones (λ = 1060 nm), respectively. The device also demonstrated external quantum efficiency (EQE) values of approximately 8.77 × 105% (λ = 520 nm) and 8.41 × 104% (λ = 1060 nm). This work achieves visible and infrared detection based on mixed-dimensional heterostructures and provides a new option for optoelectronic devices based on low-dimensional materials.

Monolayer Graphene Terahertz Detector Integrated with Artificial Microstructure.

Graphene, known for its high carrier mobility and broad spectral response range, has proven to be a promising material in photodetection applications. However, its high dark current has limited its application as a high-sensitivity photodetector at room temperature, particularly for the detection of low-energy photons. Our research proposes a new approach for overcoming this challenge by designing lattice antennas with an asymmetric structure for use in combination with high-quality monolayers of graphene. This configuration is capable of sensitive detection of low-energy photons. The results show that the graphene terahertz detector-based microstructure antenna has a responsivity of 29 V·W-1 at 0.12 THz, a fast response time of 7 µs, and a noise equivalent power of less than 8.5 pW/Hz1/2. These results provide a new strategy for the development of graphene array-based room-temperature terahertz photodetectors.

HMGA1 promotes hepatocellular carcinoma proliferation, migration, and regulates cell cycle via miR-195-5p.

HMGA1 has been reported to be aberrantly expressed and correlate with the poor prognosis of many carcinomas. This study aimed to investigate the clinical significance and molecular mechanism of HMGA1 as a tumor-suppressing gene in hepatocellular carcinoma (HCC). Analysis of TCGA dataset by TANRIC website and R2 platform, we found that HMGA1 expression was significantly higher in HCC tissues compared to that in normal liver tissues and was associated with Edmondson grade. Patients with highly expressed HMGA1 had worse overall survival. Gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes analysis showed the potential relationships between HMGA1 and other genes in HCC. We also demonstrated that the downregulation of HMGA1 dramatically suppressed the proliferation and migration of HCC cells. Furthermore, ectopic expression of HMGA1 blocked G0/G1 to S transition. Subsequent investigation characterized HMGA1 as a direct target of miR-195-5p, and miR-195-5p downregulation abrogated the effect of HMGA1 on HCC proliferation, migration, and cell cycle arrest. In addition, we also demonstrated that miR-195-5p downregulation abrogated the effect of HMGA1 on HCC growth in vivo. Taken together, our data provide strong evidence that HMGA1 promotes HCC and is negatively regulated by the tumor-suppressor, miR-195-5p.

Curcumol inhibits malignant biological behaviors and TMZ-resistance in glioma cells by inhibiting long noncoding RNA FOXD2-As1-promoted EZH2 activation.

Currently, conventional treatment is not sufficient to improve the survival of glioma patients. Hence, adopting novel personalized treatment programs is imperative. Curcumol, a Chinese herbal medicine extract from the roots of Rhizoma Curcumae, has attracted significant interest due to its beneficial pharmacological activities. The current study revealed that curcumol inhibited the proliferation, metastasis, self-renewal ability, and TMZ resistance in glioma cells in vitro and in vivo. Next, the potential molecular mechanisms of curcumol in inhibiting glioma were investigated. We found that the long non-coding RNA (lncRNA) FOXD2-As1 might contribute to the effects of curcumol on glioma cells. Enforced expression of FOXD2-As1 attenuated the curcumol-induced reduction in glioma cell proliferation, metastasis, self-renewal ability, and TMZ resistance. Moreover, the forced expression of FOXD2-As1 reversed the inhibitory effect of curcumol on the binding ability of EZH2 and H3K27me3 modification in the promoter regions of anti-oncogenes. Our results showed for the first time that curcumol is effective in inhibiting malignant biological behaviors and TMZ-resistance of glioma cells by suppressing FOXD2-As1-mediated EZH2 activation. Our study offers the possibility of exploiting curcumol as a promising therapeutic agent for glioma treatment and may provide an option for the clinical application of this natural herbal medicine.

FoxD2-AS1 is a prognostic factor in glioma and promotes temozolomide resistance in a O6-methylguanine-DNA methyltransferase-dependent manner.

Glioma is the most common brain tumor with a dismal prognosis. While temozolomide (TMZ) based chemotherapy significantly improves survival in glioma patients, resistance against this compound commonly leads to glioma treatment failure. Overexpression of long-noncoding RNA (LncRNA) FoxD2 adjacent opposite strand RNA 1 (FoxD2-AS1) was identified to promote glioma development, but the role in TMZ resistance remains unclear. In this paper, we found that FoxD2-AS1 was overexpressed in recurrent glioma, high FoxD2-AS1 expression was significantly correlated with poor patient outcome. Methylation of O6-methylguanine-DNA methyltransferase (MGMT) is significantly less frequent in high FoxD2-AS1 expression patients. Knockdown of FoxD2-AS1 decreased the proliferation, metastatic ability of glioma cells and promote the sensitivity to TMZ in glioma cells. Furthermore, knockdown of FoxD2-AS1 induced hypermethylation of the promoter region of MGMT. Our data suggested that FoxD2-AS1 is a clinical relevance LncRNA and mediates TMZ resistance by regulating the methylation status of the MGMT promoter region.