Retraction: Progressive p-channel vertical transistors fabricated using electrodeposited copper oxide designed with grain boundary tunability.

Retraction of 'Progressive p-channel vertical transistors fabricated using electrodeposited copper oxide designed with grain boundary tunability' by Sung Hyeon Jung et al., Mater. Horiz., 2022, 9, 1010-1022, https://doi.org/10.1039/D1MH01568K.

Retraction: Ambipolar operation of progressively designed symmetric bidirectional transistors fabricated using single-channel vertical transistor and electrochemically prepared copper oxide.

Retraction of 'Ambipolar operation of progressively designed symmetric bidirectional transistors fabricated using single-channel vertical transistor and electrochemically prepared copper oxide' by Sung Hyeon Jung et al., Mater. Horiz., 2023, 10, 1373-1384, https://doi.org/10.1039/D2MH01413K.

Ambipolar operation of progressively designed symmetric bidirectional transistors fabricated using single-channel vertical transistor and electrochemically prepared copper oxide.

In this study, a symmetric bidirectional transistors (SBT) is proposed. The device simultaneously implements the "strong-inversion" and "accumulation" mechanisms of a metal-oxide semiconductor field-effect transistor and TFT, respectively, in different bias directions in a single-channel vertical transistor (V-Tr). This ideal SBT device is designed and fabricated by selecting appropriate materials exhibiting a narrow bandgap and intrinsic characteristics of Sb-doped p-type Cu2O, using a V-Tr to optimize the device structure for high-field-induced short-channel and ambipolar operation, and implementing facile electrochemical deposition for channel and plasma channel treatments. To adopt artificial conductivity control for producing the transporting path of minority electron carriers, the patterned-channel-layer sidewall is locally treated using oxygen plasma, thereby suppressing the minority-carrier self-compensation. The SBT device exhibits an excellent on-current (i.e., symmetric accumulation and strong inversion modes in the p- and n-type channel regions, respectively) and excellent midregion off-current, similar to those of ideal ambipolar transistors. Moreover, owing to multilevel signals and excellent inverter behaviors, the SBT device is suitable for application in complementary-metal-oxide-semiconductors and logic memories.

Design of Functionally Stacked Channels of Oxide Thin-Film Transistors to Mimic Precise Ultralow-Light-Irradiated Synaptic Weight Modulation.

To utilize continuous ultralow intensity signals from oxide synaptic transistors as artificial synapses that mimic human visual perception, we propose strategic oxide channels that optimally utilize their advantageous functions by stacking two oxide semiconductors with different conductivities. The bottom amorphous indium-gallium-zinc oxide (a-IGZO) layer with a relatively low conductivity was designed for an extremely low initial postsynaptic current (PSCi) by achieving full depletion at a low negative gate voltage, and the stacked top amorphous indium-zinc oxide (a-IZO) layer improved the amplitude of the synaptic current and memory retention owing to the enhancement in the persistent photoconductivity characteristics. We demonstrated an excellent photonic synapse thin-film transistor (TFT) with a precise synaptic weight change even in the range of ultralow light intensity by adapting this stacking IGZO/IZO channel. The proposed device exhibited distinct ∆PSC values of 3.1 and 18.1 nA under ultralow ultraviolet light (350 nm, 50 ms) of 1.6 and 8.0 µW/cm2. In addition, while the lowest light input exhibited short-term plasticity characteristics similar to the "volatile-like" behavior of the human brain with a current recovery close to the initial value, the increase in light intensity caused long-term plasticity characteristics, thus achieving synaptic memory transition in the IGZO/IZO TFTs.

Progressive p-channel vertical transistors fabricated using electrodeposited copper oxide designed with grain boundary tunability.

A strategically designed electrodeposition method is proposed for the coating of p-type copper(i) oxide (Cu2O) channels for oxide thin film transistors. To date, conventional p-type oxide semiconductors have revealed a poor mobility and stability and this has obstructed the development of all oxide based logic devices. Furthermore, previous studies on p-type oxide transistors have been limited by the use of a typical planar type configuration. Our Cu2O electrodeposition method designed by incorporating Sb element promotes vertical alignment of the grain boundaries (GBs) and it perfectly coincides with the charge transport direction from the source to the drain in the vertical field effect transistors. These vertically aligned GBs are bundle type GBs and are likely to be ideal for vertical transistors with supreme electrical performances owing to the structurally suppressed grain boundary charge scattering. This alignment of the GBs in the electrodeposited Sb doped Cu2O (Sb:Cu2O) also demonstrates a superior vertical taper profile with conventional wet chemical etching owing to the extremely preferential etching rate along the GBs. Surprisingly, the sidewall formation, with a smooth and steep morphology causes the formation of abrupt and non-defective gate insulator/channel interfaces for superior spacer-free vertical transistors. Consequently, the Cu2O vertical field effect transistors exhibit extraordinary transistor performances of Vth = 0.4 V, µFE = 8 cm2 V-1 s-1, subthreshold swing = 0.24 V dec-1, on/off current ratio = 2 × 108 and qualified electrical and long-term stability characteristics under various environments. To the best of our knowledge, this is the first reported study on an electrodeposited method to design troublesome p-type oxide Cu2O as novel vertical transistors. Finally, power efficient logic inverter circuits with unprecedented performances, such as good noise margins, remarkable gain values of 15.6 (2 VDD) and 62.7 (5 VDD), and high frequency operation up to 10 kHz, are demonstrated using these p-type Cu2O transistors by interconnecting n-type IGZO transistors.

Ionizing radiation-inducible miR-494 promotes glioma cell invasion through EGFR stabilization by targeting p190B rhoGAP.

MicroRNAs (miRNAs) play an important role in various stages of tumor progression. miR-494, which we had previously identified as a miRNA induced by ionizing radiation (IR) in the glioma cell line U-251, was observed to enhance invasion of U-251 cells by activating MMP-2. The miR-494-induced invasive potential was accompanied by, and dependent on, epidermal growth factor receptor (EGFR) upregulation and the activation of its downstream signaling constituents, Akt and ERK. The upregulation of EGFR by miR-494 involved the suppression of lysosomal protein turnover. Among the putative target proteins tested, p190B RhoGAP (p190B) was downregulated by miR-494, and its reduced expression was responsible for the increase in EGFR expression. A reporter assay using a luciferase construct containing p190B 3'-untranslated region (3'UTR) confirmed that p190B is a direct target of miR-494. Downregulation of p190B by small interfering RNA (siRNA) transfection closely mimicked the outcomes of miR-494 transfection, and showed increased EGFR expression, MMP-2 secretion, and invasion. Ectopic expression of p190B suppressed the miR-494-induced EGFR upregulation and invasion promotion, thereby suggesting that p190B depletion is critical for the invasion-promoting action of miR-494. Collectively, our results suggest a novel function for miR-494 and its potential application as a target to control invasiveness in cancer therapy.

Phosphorylation and stabilization of c-Myc by NEMO renders cells resistant to ionizing radiation through up-regulation of γ-GCS.

The transcription factor c-Myc has been previously shown to be phosphorylated and stabilized by NEMO through direct interaction in the nucleus. Here, we show that NEMO induces up-regulation of the c-Myc target protein, γ-glutamyl-cysteine synthetase (γ-GCS), leading to an increase of intracellular glutathione (GSH) levels and simultaneous enhancement of redox-controlling capacity. NEMO enhanced c-Myc recruitment to γ-GCS promoters and c-Myc was essential for NEMO-mediated γ-GCS up-regulation. The phosphorylation and stabilization of c-Myc by NEMO rendered cells more resistant to ionizing radiation (IR). Thus, the interaction between NEMO and c-Myc may be targeted for the development of strategies to overcome the resistance to radiotherapy.

NEMO stabilizes c-Myc through direct interaction in the nucleus.

The transcription factor c-Myc is a cellular oncoprotein generally upregulated in most of human cancers. NF-κB essential modulator (NEMO) caused phosphorylation and stabilization of c-Myc protein in the nucleus through direct interaction. The interaction caused reduced ubiquitination of c-Myc by inhibiting ubiquitinating activity of Fbw7 without blocking the interaction between c-Myc and Fbw7. As a consequence, NEMO enhanced the expression of several selected c-Myc targets. Compared to the classical role as an essential subunit for the activity of IKK complex, stabilization of c-Myc by direct interaction is a unique function of NEMO, representing a new mechanism to regulate c-Myc activity.

A gonadotropin-releasing hormone-II antagonist induces autophagy of prostate cancer cells.

Gonadotropin-releasing hormone-I (GnRH-I) is known to directly regulate prostate cancer cell proliferation. However, the role of GnRH-II in prostate cancer is unclear. Here, we investigated the effect of the GnRH-II antagonist trptorelix-1 (Trp-1) on growth of PC3 prostate cancer cells. Trp-1 induced growth inhibition of PC3 cells in vitro and inhibited growth of PC3 cells xenografted into nude mice. FITC-N3, an FITC-conjugated Trp-1 analogue, was largely present in the mitochondria of prostate cancer cells, but not in other cells that are not derived from the prostate. Trp-1-induced PC3 growth inhibition was associated with decreased mitochondrial membrane potential and increased levels of mitochondrial and cytosolic reactive oxygen species (ROS). Growth inhibition was partially prevented by cotreating cells with N-acetyl cysteine, an antioxidant. Cytochrome c release and caspase-3 activation were not detected in Trp-1-treated cells. However, Trp-1 induced autophagosome formation, as seen by increased LysoTracker staining and recruitment of microtubule-associated protein 1 light chain 3 to these new lysosomal compartments. Trp-1-induced autophagy was accompanied by decreased AKT phosphorylation and increased c-Jun NH(2) terminal kinase phosphorylation, two events known to be linked to autophagy. Taken together, these data suggest that Trp-1 directly induces mitochondrial dysfunction and ROS increase, leading to autophagy of prostate cancer cells. GnRH-II antagonists may hold promise in the treatment of prostate cancer.