Targeting PERK-ATF4-P21 axis enhances the sensitivity of osteosarcoma HOS cells to Mppα-PDT.

Osteosarcoma (OS) is the most prevalent type of malignant bone tumor in adolescents. The overall survival of OS patients has reached a plateau recently. Thus, there is an urgent need to develop approaches to improve the sensitivity of OS to therapies.

Targeting X box-binding protein-1 (XBP1) enhances the sensitivity of HOS osteosarcoma cells to pyropheophorbide- α methyl ester-mediated photodynamic therapy.

Photodynamic therapy (PDT), utilizes a photochemical reaction between photosensitizer and light to cause cancer death by generating reactive oxygen species (ROS). X-box binding protein 1 (XBP1), a downstream product of the IRE1α-XBP1 pathway, regulates diverse target genes, including various proto-oncogenes and its overexpression was closely related to the occurrence and progression of malignant tumors. The present study was performed to explore the role of XBP1 in human osteosarcoma HOS cells treated with pyropheophorbide-α methyl ester (MPPα)-mediated photodynamic therapy (PDT) (MPPα-PDT) and its potential mechanisms.

RhoA enhances osteosarcoma resistance to MPPa-PDT via the Hippo/YAP signaling pathway.

Background: Osteosarcoma (OS) is the most prevalent primary bone malignancy affecting adolescents, yet the emergence of chemoradiotherapeutic resistance has limited efforts to cure affected patients to date. Pyropheophorbide-α methyl ester-mediated photodynamic therapy (MPPa-PDT) is a recently developed, minimally invasive treatment for OS that is similarly constrained by such therapeutic resistance. This study sought to explore the mechanistic basis for RhoA-activated YAP1 (YAP)-mediated resistance in OS.

Targeting GRP78 enhances the sensitivity of HOS osteosarcoma cells to pyropheophorbide-α methyl ester-mediated photodynamic therapy via the Wnt/β-catenin signaling pathway.

Photodynamic therapy (PDT), which is a new method for treating tumors, has been used in the treatment of cancer. In-depth research has shown that PDT cannot completely kill tumor cells, indicating that tumor cells are resistant to PDT. Glucose regulatory protein 78 (GRP78), which is a key regulator of endoplasmic reticulum stress, has been confirmed to be related to tumor resistance and recurrence, but there are relatively few studies on the further mechanism of GRP78 in PDT.

Antitumor effects and mechanisms of pyropheophorbide‑α methyl ester‑mediated photodynamic therapy on the human osteosarcoma cell line MG‑63.

Photodynamic therapy (PDT) is a promising treatment for osteosarcoma, and pyropheophorbide‑α methyl ester (MPPa) is a second‑generation photosensitizer for tumor treatment. The present study aimed to determine the efficacy and possible mechanisms of MPPa‑PDT in the treatment of osteosarcoma MG‑63 cells. Flow cytometry and western blotting were used to detect cell cycle‑related indicators Cyclin D1, Cyclin E, Cyclin A and Cyclin B1.

Effect and mechanisms of celastrol on the apoptosis of HOS osteosarcoma cells.

Osteosarcoma is the most common primary malignant tumor of the bone found predominantly in children and teenagers and results in early metastasis and poor prognosis. The present study primarily focused on the impact of celastrol on apoptosis and autophagy of osteosarcoma HOS cells, as well as the related mechanisms. Following the appropriate treatment, the human osteosarcoma cell line HOS was assessed for viability, Ca2+ in cells, apoptosis and changes in cell morphology using Cell Counting Kit-8, flow cytometry, inverted phase contrast microscope, Hoechst staining and transmission electron microscopy.

Establishment and characterization of human osteosarcoma cells resistant to pyropheophorbide-α methyl ester-mediated photodynamic therapy.

The present study was performed to establish and characterize new human osteosarcoma cell lines resistant to pyropheophorbide-α methyl ester‑mediated photodynamic therapy (MPPa-PDT). MPPa-PDT-resistant cells are isolated from the human osteosarcoma MG63 and HOS cell lines and two resistant populations were finally acquired, including MG63/PDT and HOS/PDT. Cell Counting Kit-8 (CCK-8) assay was used to determine the MPPa-PDT, cisplatin (CDDP) resistance and proliferation of MG63, MG63/PDT, HOS and HOS/PDT cells.