Debate over the electronic structure of CuIII complexes has intensified in recent years, focusing primarily on whether the [Cu(CF3)4]- moiety should be desc Show more
Debate over the electronic structure of CuIII complexes has intensified in recent years, focusing primarily on whether the [Cu(CF3)4]- moiety should be described as a classical Werner-type 3d8 CuIII complex or as a 3d10 CuI inverted ligand field framework. The copper periodate complex [Cu(HIO6)2]5-, discovered in 1937, has long been regarded as a 3d8 CuIII species and sometimes used as a reference 3d8 CuIII complex in oxidation state assignments for Cu-containing metalloenzymes. Nevertheless, its detailed electronic structure remains unexplored. Herein, we revisit the oxidation state of [Cu(HIO6)2]5- by means of X-ray photoelectron spectroscopy, X-ray absorption spectroscopy, and density functional theory calculations. The obtained results show that the oxidation state of the Cu center in [Cu(HIO6)2]5- lies at the boundary between the classical Werner-type and inverted ligand field regimes. This study thus demonstrates that categorizing the oxidation state of CuIII complexes as either 3d8 or 3d10 configurations is often inadequate; instead, the existence of electronic states at the boundary between these two limiting cases should be recognized. Show less
Non-small cell lung cancer (NSCLC) is one of the most prevalent and lethal types of cancers worldwide and its high incidence and mortality rates pose a significant public health challenge. Despite sig Show more
Non-small cell lung cancer (NSCLC) is one of the most prevalent and lethal types of cancers worldwide and its high incidence and mortality rates pose a significant public health challenge. Despite significant advances in targeted therapy and immunotherapy, the overall prognosis of patients with NSCLC remains poor. Hypoxia is a critical driving factor in tumor progression, influencing the biological behavior of tumor cells through complex molecular mechanisms. The present review systematically examined the role of the hypoxic microenvironment in NSCLC, demonstrating its crucial role in promoting tumor cell growth, invasion and metastasis. Additionally, it has been previously reported that the hypoxic microenvironment enhances tumor cell resistance by activating hypoxia-inducible factor and regulating exosome secretion. The hypoxic microenvironment also enables tumor cells to adapt to low oxygen and nutrient-deficient conditions by enhancing metabolic reprogramming, such as through upregulating glycolysis. Further studies have shown that the hypoxic microenvironment facilitates immune escape by modulating tumor-associated immune cells and suppressing the antitumor response of the immune system. Moreover, the hypoxic microenvironment increases tumor resistance to radiotherapy, chemotherapy and other types of targeted therapy through various pathways, significantly reducing the therapeutic efficacy of these treatments. Therefore, it could be suggested that early detection of cellular hypoxia and targeted therapy based on hypoxia may offer new therapeutic approaches for patients with NSCLC. The present review not only deepened the current understanding of the mechanisms of action and role of the hypoxic microenvironment in NSCLC but also provided a solid theoretical basis for the future development of precision treatments for patients with NSCLC. Show less