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In this work, a flexible perovskite photodetector is demonstrated with a transferable TiO2 nanorod (NR) as an electron transport layer (ETL). The TiO2 NRs are grown by the hydrothermal method on Ni metal buffer layer/Si (100) substrates. During the growth process of TiO2 NRs in solution, the Ni sacrificial buffer layer is removed by hydrochloric acid in the initial stage. The resulting suspended seed layer can then sustain the growth of TiO2 NRs in both the top and bottom directions. The successfully grown TiO2 NRs are now transferred onto an ITO‐coated PET substrate as an ETL for the flexible Cs2AgBiBr6 perovskite photodetectors. The fabricated photodetector operates under a wavelength of 405 nm, and at an external bias voltage of −0.3 V, it exhibits an outstanding performance with an on/off ratio of 1.23 × 104, photoresponsivity (R) of 0.666 A W−1, and a detectivity (D*) of 9.29 × 1012 Jones. In terms of flexibility, the optoelectronic performance of each device is well kept within 5% after 300 bending test cycles with a radius of 1 cm. The suggested transferable TiO2 NRs can improve the efficiency of flexible optoelectronic devices that require synergistic electron transfer effects by using heterostructures with TiO2 nanostructures. [ABSTRACT FROM AUTHOR]

Melatonin suppresses tumor development. However, the exact relationship between melatonin and cancer stem cells (CSCs) is poorly understood. This study found that melatonin inhibits colon CSCs by regulating the PrPC‐Oct4 axis. In specimens from patients with colorectal cancer, the expressions of cellular prion protein (PrPC) and Oct4 were significantly correlated with metastasis and tumor stages. Co‐treatment with 5‐fluorouracil (5‐FU) and melatonin inhibited the stem cell markers Oct4, Nanog, Sox2, and ALDH1A1 by downregulating PrPC. In this way, tumor growth, proliferation, and tumor‐mediated angiogenesis were suppressed. In colorectal CSCs, PRNP overexpression protects Oct4 against inhibition by 5‐FU and melatonin. In contrast, Nanog, Sox2, and ALDH1A1 have no such protection. These results indicate that PrPC directly regulates Oct4, whereas it indirectly regulates Nanog, Sox2, and ALDH1A1. Taken together, our findings suggest that co‐treatment with anticancer drug and melatonin is a potential therapy for colorectal cancer. Furthermore, PrPC maintains cancer stemness during tumor progression. Therefore, targeting the PrPC‐Oct4 axis may prove instrumental in colorectal cancer therapy. [ABSTRACT FROM AUTHOR]