Cancer Stem Cells and Drug Resistance
A topical collection in Cells (ISSN 2073-4409). This collection belongs to the section "Stem Cells".
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Editor
Topical Collection Information
Dear Colleagues,
Cancer stem cells (CSCs) are a special subgroup of tumor cells and are suggested to be responsible for drug resistance and cancer relapse, mainly due to their ability to both self-renew and resist drug targeting. In the last few years, the scientific community has dedicated significant effort to generating new strategies to eradicate this population to sensitize the tumor to new therapies. Unfortunately, this cell population still represents the cause of several treatment failures. For this collection, entitled “Cancer Stem Cells and Drug Resistance”, we welcome original research contributions that focus on advances and novel strategies to overcome drug resistance driven by cancer stem cells, as well as other challenges and new findings in the field of cancer stem cell research.
Dr. Giovanni Amabile
Guest Editor
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Published Papers (2 papers)
Open AccessBrief Report
The TIP60-CD44 Axis Modulates Colorectal Cancer Stemness
by
Asad Mohammad and Sudhakar Jha
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Abstract
HIV-1 Tat-interactive protein of 60 kDa (TIP60) is a lysine acetyltransferase protein that can acetylate histone and non-histone proteins. This study highlights TIP60’s role in regulating colorectal cancer (CRC) stemness. The depletion of
TIP60 resulted in a marked decrease in cellular proliferation, highlighting
[...] Read more.
HIV-1 Tat-interactive protein of 60 kDa (TIP60) is a lysine acetyltransferase protein that can acetylate histone and non-histone proteins. This study highlights TIP60’s role in regulating colorectal cancer (CRC) stemness. The depletion of
TIP60 resulted in a marked decrease in cellular proliferation, highlighting TIP60’s involvement in the progression of CRC. Additionally, the loss of TIP60 impacted colony formation, transitioning from densely packed structures to dispersed spindle networks along with the loss of E-cadherin, indicating its role in the epithelial–mesenchymal transition (EMT). Three-dimensional culture models suggest that TIP60 is vital for spheroid formation, highlighting its importance in maintaining cancer stem cell properties in CRC.
TIP60-depleted cells showed increased invasion in a 3D basement membrane extract (BME) invasion matrix, demonstrating its essential role in cellular invasiveness. Mechanistically, the reduction of TIP60 resulted in a decrease in
CD44 expression, a critical marker for cancer stem cells (CSCs). Notably,
CD44 overexpression restored the efficiency of spheroid formation and cell proliferation while reversing the EMT phenotype. Developing the TIP60-CD44 axis as a therapeutic target to treat CRC stemness and metastasis will help decrease the burden due to the deadly disease.
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Open AccessArticle
Pre-Clinical Assessment of SAR442257, a CD38/CD3xCD28 Trispecific T Cell Engager in Treatment of Relapsed/Refractory Multiple Myeloma
by
Anna Luise Grab, Peter S. Kim, Lukas John, Kamlesh Bisht, Hongfang Wang, Anja Baumann, Helgi Van de Velde, Irene Sarkar, Debarati Shome, Philipp Reichert, Calin Manta, Stefanie Gryzik, Rogier M. Reijmers, Niels Weinhold and Marc S. Raab
Cited by 1 | Viewed by 3548
Abstract
Current treatment strategies for multiple myeloma (MM) are highly effective, but most patients develop relapsed/refractory disease (RRMM). The anti-CD38/CD3xCD28 trispecific antibody SAR442257 targets CD38 and CD28 on MM cells and co-stimulates CD3 and CD28 on T cells (TCs). We evaluated different key aspects
[...] Read more.
Current treatment strategies for multiple myeloma (MM) are highly effective, but most patients develop relapsed/refractory disease (RRMM). The anti-CD38/CD3xCD28 trispecific antibody SAR442257 targets CD38 and CD28 on MM cells and co-stimulates CD3 and CD28 on T cells (TCs). We evaluated different key aspects such as MM cells and T cells avidity interaction, tumor killing, and biomarkers for drug potency in three distinct cohorts of RRMM patients. We found that a significantly higher proportion of RRMM patients (86%) exhibited aberrant co-expression of CD28 compared to newly diagnosed MM (NDMM) patients (19%). Furthermore, SAR442257 mediated significantly higher TC activation, resulting in enhanced MM killing compared to bispecific functional knockout controls for all relapse cohorts (Pearson’s r = 0.7). Finally, patients refractory to anti-CD38 therapy had higher levels of TGF-β (up to 20-fold) compared to other cohorts. This can limit the activity of SAR442257. Vactoserib, a TGF-β inhibitor, was able to mitigate this effect and restore sensitivity to SAR442257 in these experiments. In conclusion, SAR442257 has high potential for enhancing TC cytotoxicity by co-targeting CD38 and CD28 on MM and CD3/CD28 on T cells.
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