Qingshan Li's research while affiliated with First Affiliated Hospital of China Medical University and other places

... The research of Wong MB et al. reveals a connection between SUMO-1 and specific lysosomes in neurodegenerative diseases marked by glial protein aggregation, exemplified in multiple system atrophy and progressive supranuclear palsy(35). This association extends to glial cell models expressing α-synuclein, tau, or huntingtin exon 1 mutant, hinting at a potential role for SUMO1 in lysosomal function within the context of glioma-associated protein aggregation.Moreover, the study of Liu X sheds light on the impact of SENP1-mediated de-SUMOylation of SIRT1 in glioma development(36). This process significantly influences cell activity, cycle progression, and apoptosis through the NF-κB pathway, proposing therapeutic implications for gliomas. ...

... The co-administration with chemotherapy would lead to a less resistant population because TICs would have lost their stemness characteristics, as we discuss in the following paragraphs. The regulation of breast cancer progression through regulation of breast cancer stem cell-like properties has been recently described, probably mediated by the NF-κB cell signaling pathway [82,83], and the connection between chemoresistance, mesenchymal plasticity, and cancer stem cells in metastasis origin [84][85][86][87][88]. ...

... Other HER2 mutations include L755P (1.9%) in exon 19, V842I (0.7%) in exon 21, V659E (4.1%), and G660D (0.9%) in the transmembrane domain and D277Y (1.9%), S310F (7.7%), S310Y (1.9%), and A466V (1.4%) in the extracellular domain. 17 A list of real-world HER2 hotspots in NSCLC is shown in Table S1. The frequency of HER2 amplification varies between populations (1.4%-22%; 1.7% in Chinese). ...

... The rate of mutation to be detected or the sensitivity of mutation detection was different depending on the clinic staging. Among several studies involving advanced patients, the sensitivity ranged from 50 to 100% [34][35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50][51][52][53], However, the sensitivity was as low as 37% in studies focusing on early-stage patients [54] (Fig. 7A, Table 5). Moreover, the size of the panel used for detection also had an impact on the sensitivity. ...

... For this reason, phytochemicals or their derivatives that could be officially implemented in anti-cancer therapies are sought. The possibility of creating such drugs is demonstrated by paclitaxel and vincristine, which are compounds of plant origin used in anticancer therapy [12]. These include sanguinarine, which is representative of plant alkaloids. ...

... Furthermore, miR-361-3p could target HMGB1, which is an oncogenic molecule that has been implicated in various tumors [30][31][32][33][34][35]. High expression of HMGB1 produces the tumor-promoting role in HCC, which was capable of enhancing the growth and metastasis of HCC [36][37][38]. ...

... TPT1-AS1 is predicted to interact with miR-26a by IntaRNA software. Existing studies have revealed that miR-26a and its target HMGA1 are involved in the pathological progress of many cancers [24][25][26]. For instance, the interaction between miR-26a and its target gene HMGA1 might contribute to the malignant progression of human urothelial bladder cancer [27]. ...

... As a Chinese Food and Drug Administration-approved product, CKI has been used regularly in oncology clinics in China for more than 20 years (20,22,23). It has been used in combination with chemotherapy for the treatment of gastric, liver, and non-small cell lung carcinomas (24) and has also been observed to alleviate the toxicity of radiochemotherapy (25). ...

... Bcl-2 expression increases in NSCLC patients. This increased expression of Bcl-2 incorporated with decreased expression of Bax leads to imbalance in cell's homeostasis, which subsequently causes cancer (Alam et al., 2022;Gao et al., 2018). Caspase-3 is a mediator of apoptosis that activated during some stressful situations including exposure to cytotoxic drugs, radiotherapy, or immunotherapy (Zhou et al., 2018). ...

... It was reported that H 2 O 2 can reduce the mitochondrial membrane potential and increase the apoptotic protein expression of cleaved Caspase-3, thus inducing apoptosis in HepG2 cells. Previous studies indicated that Esc could improve oxidative stress in HEK293 cells and H9c2 cells by suppressing mitochondrial apoptosis pathways [7,19]. These findings implied that Esc improves H 2 O 2-induced oxidative stress in HepG2 cells, which might be related to inhibition of the mitochondrial apoptosis pathway. ...