Etoposide

Cells were seeded in 12-well tissue culture plates at 150,000 (Jurkat) or 200,000 (MOLM-13) cells per well. Cells were exposed to 0.1–0.5 µM etoposide (provided by the Jena University Hospital Pharmacy) for 6–48 h or to 25–400 nM palbociclib (MedChemExpress, Monmouth Junction, NJ, USA) for 48 h to induce autophagy. Cells were exposed to 2 mM 3-methyladenine (3-MA; Biomol, Hamburg, Germany) for 24 h or 48 h, or to 10 or 25 µM chloroquine (CQ; Enzo Life Sciences, Lörrach, Germany) for 1–48 h to inhibit autophagy.

U2‐OS PRDX1‐depleted and control cells (shPRDX1 & shNTC) were seeded in black Cellcarrier‐96‐well plates at 2,000 cells/well ratio and incubated overnight for attachment. The cells were treated with etoposide or carboplatin (HY‐17393, MedChem Express) at the indicated concentrations for 96 h. Plates were fixed and DAPI stained as described in the immunofluorescence microscopy section prior to cell number quantification.

CAIX inhibitor SLC-0111, developed in the laboratory of Professor Claudiu T. Supuran (NEUROFARBA Department, University of Florence, Italy) and previously described¹⁸ (link), was used at 100 µM dose to treat MSC for 24 h.
Etoposide (MedChemExpress, Sollentuna, Sweden) 100 µM was administrated to melanoma cells for 24 h to induce apoptosis.
Vemurafenib (MedChemExpress) 1 mM was used to treat for 24 h A375-M6 melanoma cells grown in standard medium or in MSC conditioned medium.

The inducible BCL6 shRNA vectors were generated based on a pLVX-TetOne-Puro vector (RRID: Addgene 124797) according to standard protocols. All constructs were verified by sequencing. shRNAs sequence targeting BCL6 are available in Supplementary file 2. Recombinant human IFN-α1 (z02866) was purchased from Genscript (Nanjing, China). Recombinant IFN-γ (300-02) and anti-human IFN-γ antibody (506532) were purchased from PeproTech (Rocky Hill, USA). Etoposide (HY-13629, a topoisomerase II inhibitor), doxorubicin (HY-15142, a topoisomerase II inhibitor), cisplatin (HY-17394, a DNA synthesis inhibitor), carboplatin (HY-17393, a DNA synthesis inhibitor), taxol (HY-B0015, a microtubule association inhibitor), and gemcitabine (HY-17026, a DNA synthesis inhibitor) were purchased from MedChemExpress (Monmouth Junction, USA).

PLX51107 was kindly provided by Plexxikon or purchased from MedChemExpress. Dinaciclib, cytarabine, etoposide, IWR-1, BML-284, and CHIR-99,021 (laduviglusib) were obtained from MedChemExpress. All chemical compounds were dissolved in Dimethyl Sulfoxide (DMSO) to prepare a 10 mM stock solution and were stored at -80 C for long-term storage as recommended.

Immortal human ESCs (T-HESC) were cultured in phenol red-free DMEM/F12 (Gibco, New York, USA) containing 10% charcoal/dextran-treated FBS (Gibco, New York, USA), 100 IU/ml penicillin (Beyotime, Shanghai, China), and 100 μg/ml streptomycin (Beyotime, Shanghai, China) at 37 °C under 5% CO₂ humidified air. Treatment included 0.5 mM 8-bromo-cAMP (MedChemExpress, Shanghai, China) and 1 μM medroxyprogesterone acetate (MPA) (MedChemExpress, Shanghai, China). In vitro artificially induced decidualization was achieved as previously described [17 ]. For decidualization experiments, confluent T-HESC monolayers were decreased in 2% DMEM/F12 media (DMEM/F12 media without phenol red, 2% FBS) overnight before treatment with 0.5 mM 8-bromo-cAMP and 1 μM medroxyprogesterone acetate (MPA). T-HESCs were induced for in vitro decidualization for 4 days using the same method described above, and the culture medium was changed every 2 days. Enzymatic activity of TOP2A was altered by treatment with 1 μM Etoposide (MedChemExpress, Shanghai, China) for 48 h.