Jing Cao

Nonmetal Methoxy‐Porphyrin Nanophotosensitizers: An Antitumor Agent for Photodynamic Therapy against Breast Cancer and Cervical Cancer

With the continuous development of precision medicine and personalized treatment, traditional therapeutic approaches such as surgery, chemotherapy, and radiotherapy are increasingly unable to meet the ever‐changing clinical needs. Therefore, developing highly efficient, low‐toxicity, and well‐targeted treatment strategies has become an urgent priority in cancer therapy. Photodynamic therapy (PDT) has made significant strides in tumor treatment in recent years. Among the various materials used in PDT, porphyrin photosensitizers have emerged as one of the most utilized options due to their exceptional photodynamic activity, excellent targeting ability, low toxicity, and versatility. Here, this study selects nonmetal methoxy‐porphyrin nanophotosensitizers as high‐performance antitumor materials. Both in vitro and in vivo analyses demonstrate that these nanophotosensitizers efficiently generate reactive oxygen species, exhibiting significant cytotoxic effects at the cellular level. In tumor‐bearing mouse models using 4T1 and HeLa cells, they show remarkable tumor inhibition, confirming their therapeutic potential in breast and cervical cancer models. Transcriptomic sequencing further reveals their regulatory roles in tumor‐related signaling pathways. Overall, these findings highlight the exceptional antitumor properties of nonmetal methoxy‐porphyrin nanophotosensitizers and provide foundational evidence for their application in PDT for gynecological malignancies.

Upregulation of SOX9 promotes the self‐renewal and tumorigenicity of cervical cancer through activating the Wnt/β‐catenin signaling pathway

Abstract Sry‐box9 (SOX9) maintains stem cell properties and plays crucial roles in many cancers. However, whether SOX9 is correlated with cervical cancer cell stemness and its detailed mechanism remains obscure. We studied the relationship between SOX9 and prognosis of cervical cancer through public database, and SOX9 was related to poor prognosis of cervical cancer. Elevated SOX9 expression enhanced the self‐renewal properties and promotes tumorigenicity in cervical cancer. Overexpression of SOX9 could promote the expression of stem cell‐related factors in cervical cancer cells and xenografts. Meanwhile, overexpression of SOX9 could also enhance the expressions of FZD10, β‐catenin, and c‐Myc in cervical cancer cells and xenografts, while inhibiting the expression of DDK1. The activation of Wnt pathway by chir‐99 021 raised the tumor spheroid ability of SOX9 knockdown HeLa cells. In addition, SOX9 could transcriptional inhibit DKK1 and activate FZD10 and MYC by binding to their promoters to affect the Wnt/β‐catenin pathway. These results demonstrated SOX9 regulated the self‐renewal and tumorigenicity of cervical cancer through Wnt/β‐catenin pathway by directly transcriptional activation of FZD10, MYC and transcriptional inhibition of DKK1.