Nonresonant hyper‐Raman and hyper‐Rayleigh scattering in benzene and pyridine

This is the publisher's version, also available electronically from http://scitation.aip.org/content/aip/journal/jcp/90/9/10.1063/1.456592.Nonresonant hyper‐Raman and hyper‐Rayleigh spectra excited at 1064 nm are reported for neat benzene and pyridine. The theory of Herzberg–Teller vibronic coupling in nonresonant and preresonant hyper‐Raman scattering is developed. Nonresonant hyper‐Raman scattering is shown to be vibronically induced by modes that efficiently couple strongly allowed one‐photon and two‐photon transitions. A weak and broad (55 cm− 1) hyper‐Rayleigh band was observed in benzene and attributed to collective scattering, while in pyridine, a much more intense and much narrower hyper‐Rayleigh band was observed. Only the a 2u vibration (ν1 1) was observed in the hyper‐Raman spectrum of benzene, while several strong bands were observed in pyridine. Possible vibronic‐coupling pathways are discussed for these modes. In addition, the observed hyper‐Raman spectrum of pyridine is compared to a recent calculation

Regulation of glioma cell invasion by 3q26 gene products PIK3CA, SOX2 and OPA1

Diffuse gliomas progress by invading neighboring brain tissue to promote post-operative relapse. Transcription factor SOX2 is highly expressed in invasive gliomas and maps to chromosome region 3q26 together with the genes for PI3K/AKT signaling activator PIK3CA and effector molecules of mitochondria fusion and cell invasion, MFN1 and OPA1. Gene copy number analysis at 3q26 from 129 glioma patient biopsies revealed mutually exclusive SOX2 amplifications (26%) and OPA1 losses (19%). Both forced SOX2 expression and OPA1 inactivation increased LN319 glioma cell invasion in vitro and promoted cell dispersion in vivo in xenotransplanted D. rerio embryos. While PI3 kinase activity sustained SOX2 expression, pharmacological PI3K/AKT pathway inhibition decreased invasion and resulted in SOX2 nucleus-to-cytoplasm translocation in a mTORC1-independent manner. Chromatin immuno-precipitation and luciferase reporter gene assays together demonstrated that SOX2 trans-activates PIK3CA and OPA1. Thus, SOX2 activates PI3K/AKT signaling in a positive feedback loop, while OPA1 deletion is interpreted to counter-act OPA1 trans-activation. Remarkably, neuro-imaging of human gliomas with high SOX2 or low OPA1 genomic imbalances revealed significantly larger necrotic tumor zone volumes, corresponding to higher invasive capacities of tumors, while autologous necrotic cells are capable of inducing higher invasion in SOX2 overexpressing or OPA1 knocked-down relative to parental LN319. We thus propose necrosis volume as a surrogate marker for the assessment of glioma invasive potential. Whereas glioma invasion is activated by a PI3K/AKT-SOX2 loop, it is reduced by a cryptic invasion suppressor SOX2-OPA1 pathway. Thus, PI3K/AKT-SOX2 and mitochondria fission represent connected signaling networks regulating glioma invasion. This article is protected by copyright. All rights reserved