![In vitro anticancer activity of MIR17PTi. (A) CCK-8 assay of CCLs (n = 48) and nonmalignant cell lines (NM-CLs; n = 5) exposed for 6 days to MIR17PTi or scr-NC (10 µM). Data are represented as percentage of MIR17PTi-treated live cells (absorbance), as compared with scr-NC. Dashed lines indicate 20% (upper line) and 80% (bottom line) growth inhibition. (B) CCK-8 proliferation assay of 8 CCLs (P3HR1 [diffuse large B cell lymphoma (DLBCL)], SULTAN [Burkitt lymphoma (BL)], JeKo-1, Maver [mantle cell lymphoma (MCL)], AMO1, KMS-12-BM, NCI-H929, RPMI-8226 [MM]) transfected with indicated miRNA inhibitors or MIR17PTi (25 nM). Data are represented as compared (percentage) with live cells after scr-NC transfection. (C) CCK-8 proliferation assay of RPMI-8226 and AMO1 after transfection with miR-NC-inhibitors (150 nM) or pooled miR-17-92 inhibitors (25 nM each) or scr-NC (25 nM) or MIR17PTi (25 nM). Data are represented as compared (percentage) with live cells after mock (RNase-free water) transfection. (D) CCK-8 proliferation assay of: AMO1 2 days after cotransfection with scr-NC (5 or 25 nM; showed as single point because no difference was detected in percentage of live cells) or MIR17PTi (5 or 25 nM) and miR-NC-mimics (60 nM) or pooled miR-17-92 mimics (10 nM each) (left) and AMO1 transduced with an empty lentiviral vector or an miR-17-92 lentiviral vector and then exposed for 6 days to scr-NC or MIR17PTi (0.5 µM) (right). Data from 1 of 3 independent experiments are shown in each panel. *P < .05. AML, acute myeloid leukemia; BC, breast cancer; MPM, malignant pleural mesothelioma; PC, pancreatic cancer; TCL, T-cell leukemia.](https://ash.silverchair-cdn.com/ash/content_public/journal/blood/132/10/10.1182_blood-2018-03-836601/4/blood836601f2.jpeg?Expires=1721523444&Signature=klEcYzOPJebAvqeMq5UwVLmLRVxAA~2Yk0c6GWRsZKHQzJaZ~2~Hzn2zBXcPeTnaddl51i2NqfoSo7HgT2OxcQJHgGnlkuxOnm89Zhg4uJNJhIaGXjnlL6RlU5UEu739m~aqAAJ~BShz31Xm8GrqVf0h4x4U-bptYeG7VL~HKdOLhjHY0fjatdV8hox0mDswolBAzgXfjAiaD6xWCdTUk7zR2QN~PyDZCVmrOx91g-hIJi67pig0MN~KQ0DwUREBQmviiA3ZsOK1XCmwyJRy6aGXa447EwwCiUaeqGPaEAa8NZwmjW7Fx5MJDhk8KCJxaHig9-qhfeM7p7Psio7jng__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
In vitro anticancer activity of MIR17PTi. (A) CCK-8 assay of CCLs (n = 48) and nonmalignant cell lines (NM-CLs; n = 5) exposed for 6 days to MIR17PTi or scr-NC (10 µM). Data are represented as percentage of MIR17PTi-treated live cells (absorbance), as compared with scr-NC. Dashed lines indicate 20% (upper line) and 80% (bottom line) growth inhibition. (B) CCK-8 proliferation assay of 8 CCLs (P3HR1 [diffuse large B cell lymphoma (DLBCL)], SULTAN [Burkitt lymphoma (BL)], JeKo-1, Maver [mantle cell lymphoma (MCL)], AMO1, KMS-12-BM, NCI-H929, RPMI-8226 [MM]) transfected with indicated miRNA inhibitors or MIR17PTi (25 nM). Data are represented as compared (percentage) with live cells after scr-NC transfection. (C) CCK-8 proliferation assay of RPMI-8226 and AMO1 after transfection with miR-NC-inhibitors (150 nM) or pooled miR-17-92 inhibitors (25 nM each) or scr-NC (25 nM) or MIR17PTi (25 nM). Data are represented as compared (percentage) with live cells after mock (RNase-free water) transfection. (D) CCK-8 proliferation assay of: AMO1 2 days after cotransfection with scr-NC (5 or 25 nM; showed as single point because no difference was detected in percentage of live cells) or MIR17PTi (5 or 25 nM) and miR-NC-mimics (60 nM) or pooled miR-17-92 mimics (10 nM each) (left) and AMO1 transduced with an empty lentiviral vector or an miR-17-92 lentiviral vector and then exposed for 6 days to scr-NC or MIR17PTi (0.5 µM) (right). Data from 1 of 3 independent experiments are shown in each panel. *P < .05. AML, acute myeloid leukemia; BC, breast cancer; MPM, malignant pleural mesothelioma; PC, pancreatic cancer; TCL, T-cell leukemia.
