Song Wu

Dr. Song Wu


Research Focus & Metrics

Academic Career Length

20Years (2007-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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18 January 2023 in Cancers
Verified
Journal Article
Open access
PDF file
WJwenqi jiang
wenqi jiang
MLMingKang Liang
MingKang Liang
QLQifang Lei
Qifang Lei
GLGuang-Zhi Li
Guang-Zhi Li
SWSong Wu
Song Wu
Although we have made great strides in treating deadly diseases over the years, cancer therapy still remains a daunting challenge. Among numerous anticancer methods, photodynamic therapy (PDT), a non-invasive therapeutic approach, has attracted much attention. PDT exhibits outstanding performance in cancer therapy, but some unavoidable disadvantages, including limited light penetration depth, poor tumor selectivity, as well as oxygen dependence, largely limit its therapeutic efficiency for solid tumors treatment. Thus, numerous strategies have gone into overcoming these obstacles, such as exploring new photosensitizers with higher photodynamic conversion efficiency, alleviating tumor hypoxia to fuel the generation of reactive oxygen species (ROS), designing tumor-targeted PS, and applying PDT-based combination strategies. In this review, we briefly summarized the PDT related tumor therapeutic approaches, which are mainly characterized by advanced PSs, these PSs have excellent conversion efficiency and additional refreshing features. We also briefly summarize PDT-based combination therapies with excellent therapeutic effects.

8 January 2025 in Nature Medicine
Verified
Journal Article
Closed access
PDF file
XLXiaohong Liu
Xiaohong Liu
HLHao Liu
Hao Liu
GYGuoxing Yang
Guoxing Yang
ZJZeyu Jiang
Zeyu Jiang
SCShuguang Cui
Shuguang Cui
GWGuangyu Wang
Guangyu Wang

3 May 2023 in Signal Transduction and Targeted Therapy
Verified
Journal Article
Open access
PDF file
TWThian-Sze Wong
Thian-Sze Wong
GLGuangzhi Li
Guangzhi Li
SLShiliang Li
Shiliang Li
WGWei Gao
Wei Gao
GCGeng Chen
Geng Chen
YDYang Du
Yang Du
Neuropsychiatric disorders are multifactorial disorders with diverse aetiological factors. Identifying treatment targets is challenging because the diseases are resulting from heterogeneous biological, genetic, and environmental factors. Nevertheless, the increasing understanding of G protein-coupled receptor (GPCR) opens a new possibility in drug discovery. Harnessing our knowledge of molecular mechanisms and structural information of GPCRs will be advantageous for developing effective drugs. This review provides an overview of the role of GPCRs in various neurodegenerative and psychiatric diseases. Besides, we highlight the emerging opportunities of novel GPCR targets and address recent progress in GPCR drug development.

19 February 2019 in Molecular Cancer
Verified
Journal Article
Open access
PDF file
HSHongwei Su
Hongwei Su
TTTao Tao
Tao Tao
ZYZhao Yang
Zhao Yang
JKJason Xing KANG
Jason Xing KANG
XZXu Zhang
Xu Zhang
CLChong Li
Chong Li
Circular RNA (circRNA) represents a broad and diverse endogenous RNAs that can regulate gene expression in cancer. However, the regulation and function of bladder cancer (BC) circRNAs remain largely unknown. Here we generated circRNA microarray data from three BC tissues and paired non-cancerous matched tissues, and detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. We subsequently performed functional analyses in cell lines and an animal model to support clinical findings. Mechanistically, we demonstrated that cTFRC could directly bind to miR-107 and relieve suppression for target TFRC expression. We detected circular RNA-cTFRC up-regulated and correlated with tumor grade and poor survival rate of BC patients. Knock down of cTFRC inhibited invasion and proliferation of BC cell lines in vitro and tumor growth in vivo. Furthermore, the expression of cTFRC correlated with TFRC and negatively correlated with miR-107 both in BC cell lines and BC clinical samples. In addition, up-regulation of cTFRC promoted TFRC expression and contributed to an epithelial to mesenchymal transition phenotype in BC cells. Finally, we found that cTFRC acts as a competing endogenous RNA (ceRNA) for miR-107 to regulate TFRC expression. cTFRC may exert regulatory functions in BC and may be a potential marker of BC diagnosis or progression.

1 January 2017 in European Urology
Verified
Journal Article
Open access
ZYZhao Yang
Zhao Yang
CLChong Li
Chong Li
ZFZusen Fan
Zusen Fan
HLHongjie Liu
Hongjie Liu
XZXiaolong Zhang
Xiaolong Zhang
SWSong Wu
Song Wu
Cancer stem cells are considered responsible for many important aspects of tumors such as their self-renewal, tumor-initiating, drug-resistance and metastasis. However, the genetic basis and origination of human bladder cancer stem cells (BCSCs) remains unknown. Here, we conducted single-cell sequencing on 59 cells including BCSCs, bladder cancer non-stem cells (BCNSCs), bladder epithelial stem cells (BESCs) and bladder epithelial non-stem cells (BENSCs) from three bladder cancer (BC) specimens. Specifically, BCSCs demonstrate clonal homogeneity and suggest their origin from BESCs or BCNSCs through phylogenetic analysis. Moreover, 21 key altered genes were identified in BCSCs including six genes not previously described in BC (ETS1, GPRC5A, MKL1, PAWR, PITX2 and RGS9BP). Co-mutations of ARID1A, GPRC5A and MLL2 introduced by CRISPR/Cas9 significantly enhance the capabilities of self-renewal and tumor-initiating of BCNSCs. To our knowledge, our study first provides an overview of the genetic basis of human BCSCs with single-cell sequencing and demonstrates the biclonal origin of human BCSCs via evolution analysis. Human bladder cancer stem cells show the high level of consistency and may derived from bladder epithelial stem cells or bladder cancer non-stem cells. Mutations of ARID1A, GPRC5A and MLL2 grant bladder cancer non-stem cells the capability of self-renewal.

8 August 2019 in Advanced Functional Materials
Verified
Journal Article
Closed access
PDF file
GLGuangzhi Li
Guangzhi Li
SYSimin Yuan
Simin Yuan
DDDashi Deng
Dashi Deng
TOTong Ou
Tong Ou
YLYuqing Li
Yuqing Li
SWSong Wu
Song Wu