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PO Tetrahedron Assisted Chelate Engineering for 10.67%-Efficient Antimony Selenosulfide Solar Cells.

Adv Mater

January 2025

Institute of Thin Film Physics and Applications, Shenzhen Key Laboratory of Advanced Thin Films and Applications, Key Laboratory of Optoelectronic Devices and Systems of Ministry of Education and Guangdong Province, State Key Laboratory of Radio Frequency Heterogeneous Integration, College of Physics and Optoelectronic Engineering, Shenzhen University, Shenzhen, 518060, China.

Anisotropic carrier transport and deep-level defect of antimony selenosulfide (Sb(S,Se)) absorber are two vital auses restraining the photovoltaic performance of this emerging thin-film solar cell. Herein, chelate engineering is proposed to prepare high-quality Sb(S,Se) film based on hydrothermal deposition approach, which realizes desirable carrier transport and passivated defects by using tetrahedral PO ion in dibasic sodium phosphate (NaHPO, DSP). The PO Lewis structure, on one hand in the form of [(SbO)(PO)] chelate, can adsorb on the polar planes of cadmium sulfide (CdS) layer, promoting the heterogeneous nucleation, and on the other hand, the tetrahedral PO inhibits horizontal growth of (SbS(e)) ribbons due to size effects, thus achieving desirable [hk1] orientation.

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Aim: Breast cancer (BC) is the most frequently diagnosed malignancy worldwide, necessitating continued research into its molecular mechanisms. Circular RNAs (circRNAs) are increasingly recognized for their role in various cancers, including BC. This study explores the role of circRNA kinesin family member 4A (circKIF4A) in BC progression and its underlying molecular mechanisms.

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Heteronemin suppresses EGF‑induced proliferation through the PI3K/PD‑L1 signaling pathways in cholangiocarcinoma.

Oncol Rep

March 2025

Graduate Institute of Nanomedicine and Medical Engineering, College of Medical Engineering, Taipei Medical University, Taipei 11031, Taiwan, R.O.C.

Epidermal growth factor (EGF) binds with its surface receptor to stimulate gene expression and cancer cell proliferation. EGF stimulates cancer cell growth via phosphoinositide 3‑kinase (PI3K) and programmed cell death ligand 1 (PD‑L1) pathways. As an integrin αvβ3 antagonist, heteronemin exhibits potent cytotoxic effects against cancer cells.

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Human papillomavirus (HPV)‑positive and -negative head and neck squamous cell carcinoma (HNSCC) are often associated with activation of the phosphatidylinositol 3‑kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway due to mutations or amplifications in , loss of or activation of receptor tyrosine kinases. In HPV‑negative tumors, (encoding p16 protein) inactivation or (encoding Cyclin D1 protein) amplification frequently results in sustained cyclin‑dependent kinase (CDK) 4/6 activation. The present study aimed to investigate the efficacy of the CDK4/6 inhibitors (CDKi) palbociclib and ribociclib, and the PI3K/Akt/mTOR pathway inhibitors (PI3Ki) gedatolisib, buparlisib and alpelisib, in suppressing cell viability of HPV‑positive and ‑negative HNSCC cell lines.

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Pancreatic cancer is an aggressive tumor, which is often associated with a poor clinical prognosis and resistance to conventional chemotherapy. Therefore, there is a need to identify new therapeutic markers for pancreatic cancer. Although KIN17 is a highly expressed DNA‑ and RNA‑binding protein in a number of types of human cancer, its role in pancreatic cancer development, especially in relation to progression, is currently unknown.

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