2020
DOI: 10.2147/cmar.s278012
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SLAMF1 Promotes Methotrexate Resistance via Activating Autophagy in Choriocarcinoma Cells

Abstract: The acquisition of chemoresistance to methotrexate (MTX) still remains one of the major challenges for choriocarcinoma treatment. Herein, we aimed to evaluate the potential role of Signaling Lymphocytic Activation Molecule Family Member 1 (SLAMF1) as a possible regulator of chemoresistance to MTX in choriocarcinoma. Material and Methods: MTX-resistant JEG3 and JAR sublines (JEG3/MTX, JAR/MTX) were used to study SLAMF1 function. CCK8 assay and soft agar assay were conducted to measure the cell viability and clo… Show more

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Cited by 10 publications
(7 citation statements)
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“…It should be noted that ROS can activate both autophagy and apoptosis. In contrast to apoptosis, autophagy can promote the progression of cancer cells [332]. Therefore, if autophagy activation occurs following pharmacological intervention and enhancing ROS levels in CP chemotherapy, the exact role of autophagy should be determined, and if autophagy functions as a pro-survival mechanism, autophagy inhibitors, such as chloroquine can be utilized.…”
Section: Conclusion and Remarksmentioning
confidence: 99%
“…It should be noted that ROS can activate both autophagy and apoptosis. In contrast to apoptosis, autophagy can promote the progression of cancer cells [332]. Therefore, if autophagy activation occurs following pharmacological intervention and enhancing ROS levels in CP chemotherapy, the exact role of autophagy should be determined, and if autophagy functions as a pro-survival mechanism, autophagy inhibitors, such as chloroquine can be utilized.…”
Section: Conclusion and Remarksmentioning
confidence: 99%
“…LAT2 promotes the progression of multiple tumors and drug resistance (47,48). SLAMF1 promotes methotrexate resistance by activating autophagy of choriocarcinoma cells (49). Moreover, it serves as a prognostic marker gene of chronic lymphoblastic leukemia (CLL) (50,51).…”
Section: Discussionmentioning
confidence: 99%
“…Correctly assessing and predicting GTN chemoresistance, exploring the relevant molecular mechanisms of chemoresistance, and searching for chemoresistance predictors and potential therapeutic targets are urgent clinical needs. Previous studies have confirmed that MTX resistance is related to a variety of molecules, such as ABC transporter and multidrug resistance-related protein (MRP1) pumping out drugs, resulting in a decrease in intracellular drug concentrations ( 11 ). Dipeptidyl peptidase-4 (DPP4), methyltransferase-like protein 7A (METTL7A), and transcription factor SOX8 may promote MTX resistance by activating pro-survival signaling pathways and reducing the accumulation of reactive oxygen species (ROS) in JEG3 cells ( 12 ).…”
Section: Discussionmentioning
confidence: 99%