A high-performance switchable 0.612 nm-spaced dual-wavelength erbium-doped fiber (EDF) laser is proposed and experimentally demonstrated. For the first time, we combine a compound-cavity structure (CCS) and an enhanced polarization hole burning (PHB) effect in laser cavity to obtain stable dual-wavelength lasing (λ1 and λ2) and single-longitudinal-mode (SLM) operation at each wavelength without mode-hopping. In the CCS, a high-quality triple-ring passive-resonator is employed to achieve SLM lasing and a high-birefringence fiber Bragg grating combined with a three-loop polarization controller made with a length of EDF is used to establish strong PHB effect. Easy switch between dual- and single-wavelength lasing modes is achieved. At a pump power of 150 mW, we obtain dual-wavelength lasing with optical signal to noise ratios (OSNRs) of >84 dB for both wavelengths and linewidths of 663 Hz for λ1 and 768 Hz for λ2 respectively; we also obtain single-wavelength lasing at λ1 with an OSNR of >86 dB and a linewidth of 687 Hz or at λ2 with an OSNR of >88 dB and a linewidth of 678 Hz. For both dual- and single-wavelength operations, the two lasing wavelengths are orthogonally polarized, with a degree of polarization of ∼100%, and their relative intensity noise are <-155 dB/Hz at frequencies over 3 MHz. In addition, the dependences of wavelength, OSNR and linewidth on pump power and wavelength-tunability on temperature for the proposed fiber laser are also investigated in detail.

5-aminolevulinic acid (5-ALA) is a precursor of the photosensitizer and photodynamic therapy (PDT) has been used in clinical practice. However, tumor cellular hypoxia severely affects the efficiency of photodynamic therapy. In this study, photodynamic therapy was combined with tirapazamine to investigate the effects of the combined intervention and the related mechanisms it may involve. Colony formation assays were used to demonstrate cell proliferation. Transwell assays were performed to observe the effect on cell invasion and metastasis after the corresponding intervention. DCFH-DA probe was used to detect the reactive oxygen species content. Flow cytometry was used to detect the effects of the interventions on apoptosis and cell cycle. The relevant pathways that may be involved are explored by examining the expression levels of the relevant proteins and genes. Colony formation assays indicated that the combined intervention inhibited cell proliferation. Transwell assays demonstrated that PDT combined with TPZ effectively inhibited tumor cell invasion and metastasis. In addition, fluorescence intensity generated by DCFH-DA oxidation was detected indicating that the combined intervention increased the formation of reactive oxygen species. Flow cytometry clearly showed that the combination of PDT and TPZ further increased apoptosis and cell cycle arrest. The results of western blotting and qRT-PCR experiments confirmed that the combination therapy inhibited HIF-1α/VEGF axis and the PI3K/Akt/mTOR pathway activation. 5-ALA-PDT combined with TPZ can inhibit cell proliferation, increase apoptosis, and inhibit the PI3K/Akt/mTOR pathway, thus inhibiting tumor growth and metastasis and improving anti-cancer effects.

Introduction: Cisplatin resistance is a major challenge in ovarian cancer therapy, particularly for high-grade serous ovarian cancer (HGSOC). DNA topoisomerase IIα (TOP2A) relates to cancer drug resistance, yet its role and molecular mechanisms in ovarian cancer cisplatin resistance remain unclear. Methods: TOP2A expression was detected in HGSOC tissues and cisplatin-resistant cells (SKOV3-DDP, OVCAR3-DDP). Functional assays combined with TOP2A knockdown evaluated cisplatin sensitivity and malignant phenotypes (proliferation, invasion, migration) in resistant cells. RNA-seq and GEO cisplatin resistance dataset (GSE214302) validated TOP2A’s role in cisplatin resistance, prognostic value, and associations with TP53, GPX4, SLC7A11. Molecular docking/Co-IP confirmed TOP2A-TP53 interaction. Fer-1 and TP53 knockdown clarified TP53/GPX4/SLC7A11 axis regulation of ferroptosis and EMT, and an in vivo xenograft tumor model validated these findings. Results: TOP2A is highly expressed in HGSOC tissues and cisplatin-resistant cells, with high levels strongly associated with tumor progression (advanced stage, high grade, lymph node metastasis) and poor prognosis. RNA-seq shows TOP2A correlates with TP53, GPX4, SLC7A11.GEO dataset analysis confirms all four associate with cisplatin resistance. SLC7A11 and TOP2A are effective resistance biomarkers, and high TOP2A predicts shorter progression-free survival. Molecular assays verify direct TOP2A-TP53 interaction. Functional experiments reveal TOP2A knockdown enhances cisplatin sensitivity, inhibits malignancy, activates ferroptosis, and suppresses EMT via the TP53/GPX4/SLC7A11 axis. This effect is reversed by Fer-1 or TP53 knockdown, with mechanisms validated in vivo . Conclusion: TOP2A represents a potential prognostic biomarker and therapeutic target for cisplatin resistance in ovarian cancer (OC), as it regulates ferroptosis and EMT via the TP53/GPX4/SLC7A11 axis, which is mediated by its direct interaction with TP53. This thus provides a novel direction for treating cisplatin-resistant OC.