C-Myc inhibition intensified the anti-leukemic properties of Imatinib in chronic myeloid leukemia cells

S Zehtabcheh, AM Yousefi, M Momeny… - Molecular Biology …, 2023 - Springer
Background Due to its remarkable efficacy in producing hematologic, cytogenetic, and
molecular remissions, the FDA approved Imatinib as the first-line treatment for newly …

[引用][C] Connexin-43 prevents hematopoietic stem cell senescence through transfer of reactive oxygen species to bone marrow stromal cells

ET Ishikawa, D Gonzalez-Nieto… - … of the National …, 2012 - NATL ACAD SCIENCES 2101 …

[HTML][HTML] Bone marrow mesenchymal stromal cells non-selectively protect chronic myeloid leukemia cells from imatinib-induced apoptosis via the CXCR4/CXCL12 axis

F Vianello, F Villanova, V Tisato, S Lymperi, KK Ho… - …, 2010 - ncbi.nlm.nih.gov
Background Residual chronic myeloid leukemia disease following imatinib treatment has
been attributed to the presence of quiescent leukemic stem cells intrinsically resistant to …

[HTML][HTML] In vitro inhibited effect of gap junction composed of Cx43 in the invasion and metastasis of testicular cancer resistanced to cisplatin

D Wu, B Li, H Liu, M Yuan, M Yu, L Tao, S Dong… - Biomedicine & …, 2018 - Elsevier
The effect of gap junction intercellular communication composed of connexin on cancer
invasion/metastasis has been thoroughly explored; however, its effect on testicular cancer …

[HTML][HTML] Specific and targetable interactions with the bone marrow microenvironment govern outcome in imatinib-resistant chronic myeloid leukemia

R Kumar, M Marten, V Minciacchi, R Pereira, C Zanetti… - Blood, 2018 - Elsevier
Mutations within BCR-ABL1, the oncogene giving rise to chronic myeloid leukaemia (CML),
can lead to resistance to tyrosine kinase inhibitors and some are associated with clinically …

CAY10683 and imatinib have synergistic effects in overcoming imatinib resistance via HDAC2 inhibition in chronic myeloid leukemia

T Zhang, D Wei, T Lu, D Ma, K Yu, Q Fang, Z Zhang… - RSC …, 2020 - pubs.rsc.org
Imatinib (IM) is utilized for targeting the BCR–ABL fusion protein and as such, chronic
myeloid leukemia (CML) is considered to be a curable disorder for which patients can …

Increased interaction between connexin43 and microtubules is critical for glioblastoma stem-like cell maintenance and tumorigenicity.

JW Smyth, S Guo, L O'Rourke, S Deaver, J Dahlka… - bioRxiv, 2024 - biorxiv.org
Glioblastoma (GBM) is the most common primary tumor of the central nervous system. One
major challenge in GBM treatment is the resistance to chemotherapy and radiotherapy …

Effect of Cx43 on proliferation of C6 glioma cells and its mechanisms

Y LI, X Pang, M LI, Q Wang, Y Yang… - Chinese …, 2017 - pesquisa.bvsalud.org
Aim To explore the effect of Cx43 over-expression on proliferation of C6 cells and its
mechanisms by transfecting pCMV-Cx43cDNA plasmid into C6 cells. Methods pCMV …

Detection of Cx43 and P27 in acute myeloid leukemia patients with t (8; 21)

SBM El-Hady, E Almasry… - The Egyptian Journal of …, 2012 - journals.lww.com
Background Connexin 43 (Cx43) inhibits cell proliferation in gap junction-dependent and
gap junction-independent mechanisms and contributes to the pathogenesis of many …

The carboxy-terminal domain of connexin 43 (CT-Cx43) modulates the expression of p53 by altering miR-125b expression in low-grade human breast cancers

R Maqbool, R Rashid, R Ismail, S Niaz, NA Chowdri… - Cellular oncology, 2015 - Springer
Abstract Purpose Connexin 43 (Cx43) is a widely expressed gap junction protein. It can also
regulate various gap-junction independent processes, including cellular proliferation. The …