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BUFFALO, NY- May 20, 2024 – A new research paper was published in Oncotarget's Volume 15 on May 16, 2024, entitled, “The anticancer potential of the CLK kinases inhibitors 1C8 and GPS167 revealed by their impact on the epithelial-mesenchymal transition and the antiviral immune response.”

The diheteroarylamide-based compound 1C8 and the aminothiazole carboxamide-related compound GPS167 inhibit the CLK kinases, and affect the proliferation of a broad range of cancer cell lines. A chemogenomic screen previously performed with GPS167 revealed that the depletion of components associated with mitotic spindle assembly altered sensitivity to GPS167.
 
In this new study, researchers Lulzim Shkreta, Johanne Toutant, Aurélie Delannoy, David Durantel, Anna Salvetti, Sophie Ehresmann, Martin Sauvageau, Julien A. Delbrouck, Alice Gravel-Trudeau, Christian Comeau, Caroline Huard, Jasmin Coulombe-Huntington, Mike Tyers, David Grierson, Pierre-Luc Boudreault, and Benoit Chabot from Université de Sherbrooke, Université de Lyon, Institut de recherches cliniques de Montréal, Université de Montréal, and University of British Columbia a similar screen performed with 1C8 also established the impact of components involved in mitotic spindle assembly. 

“Accordingly, transcriptome analyses of cells treated with 1C8 and GPS167 indicated that the expression and RNA splicing of transcripts encoding mitotic spindle assembly components were affected.” 

The functional relevance of the microtubule connection was confirmed by showing that subtoxic concentrations of drugs affecting mitotic spindle assembly increased sensitivity to GPS167. 1C8 and GPS167 impacted the expression and splicing of transcripts in pathways relevant to tumor progression, including MYC targets and the epithelial mesenchymal transition (EMT). Finally, 1C8 and GPS167 altered the expression and alternative splicing of transcripts involved in the antiviral immune response. Consistent with this observation, depleting the double-stranded RNA sensor DHX33 suppressed GPS167-mediated cytotoxicity on HCT116 cells. 

“Our study uncovered molecular mechanisms through which 1C8 and GPS167 affect cancer cell proliferation as well as processes critical for metastasis."

DOI - https://doi.org/10.18632/oncotarget.28585

Correspondence to - Benoit Chabot - benoit.chabot@usherbrooke.ca

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Keywords - cancer, CLK kinases inhibitors, EMT, antiviral immune response, microtubules, metastasis

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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Oncotarget

Anticancer Potential of CLK Kinase Inhibitors 1C8 and GPS167 via EMT and Antiviral Immune Response

Dr. Benoit Chabot from Université de Sherbrooke in Quebec, CA, discusses a research paper he co-authored that was published by Oncotarget in Volume 15, entitled, “The anticancer potential of the CLK kinases inhibitors 1C8 and GPS167 revealed by their impact on the epithelial-mesenchymal transition and the antiviral immune response.”

DOI - https://doi.org/10.18632/oncotarget.28585

Correspondence to - Benoit Chabot - benoit.chabot@usherbrooke.ca

Video interview - https://www.youtube.com/watch?v=zAnSZ0oycDY

Transcription - https://www.oncotarget.net/2024/05/30/behind-the-study-anticancer-potential-of-clk-kinase-inhibitors-1c8-and-gps167/

Abstract

The diheteroarylamide-based compound 1C8 and the aminothiazole carboxamide-related compound GPS167 inhibit the CLK kinases, and affect the proliferation of a broad range of cancer cell lines. A chemogenomic screen previously performed with GPS167 revealed that the depletion of components associated with mitotic spindle assembly altered sensitivity to GPS167. Here, a similar screen performed with 1C8 also established the impact of components involved in mitotic spindle assembly. Accordingly, transcriptome analyses of cells treated with 1C8 and GPS167 indicated that the expression and RNA splicing of transcripts encoding mitotic spindle assembly components were affected. The functional relevance of the microtubule connection was confirmed by showing that subtoxic concentrations of drugs affecting mitotic spindle assembly increased sensitivity to GPS167. 1C8 and GPS167 impacted the expression and splicing of transcripts in pathways relevant to tumor progression, including MYC targets and the epithelial mesenchymal transition (EMT). Finally, 1C8 and GPS167 altered the expression and alternative splicing of transcripts involved in the antiviral immune response. Consistent with this observation, depleting the double-stranded RNA sensor DHX33 suppressed GPS167-mediated cytotoxicity on HCT116 cells. Our study uncovered molecular mechanisms through which 1C8 and GPS167 affect cancer cell proliferation as well as processes critical for metastasis.

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Keywords - cancer, CLK kinases inhibitors, EMT, antiviral immune response, microtubules, metastasis

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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Behind the Study: Anticancer Potential of CLK Kinase Inhibitors 1C8 and GPS167

BUFFALO, NY- June 18, 2024 – A new #research perspective was #published in Oncotarget's Volume 15 on June 13, 2024, entitled, “When does a melanoma metastasize? Implications for management.”

In this new perspective, researchers John F. Thompson and Gabrielle J. Williams from The University of Sydney, Royal Prince Alfred Hospital, and the University of Western Australia discussed melanoma and timing treatment. Selecting which patients with clinically localized melanoma require treatment other than wide excision of the primary tumor is based on the risk or presence of metastatic disease. This in turn is linked to survival. 

“Knowing if and when a melanoma is likely to metastasize is therefore of great importance.” 

Several studies employing a range of different methodologies have suggested that many melanomas metastasize long before the primary lesion is diagnosed. Therefore, waiting for dissemination of metastatic disease to become evident before making systemic therapy available to these patients may be less effective than giving them post-operative adjuvant therapy initially if the metastatic risk is high. The identification of these high-risk patients will assist in selecting those to whom adjuvant systemic therapy can most appropriately be offered. 

“Further studies are required to better identify high-risk patients whose primary melanoma is likely to have already metastasized.”

DOI - https://doi.org/10.18632/oncotarget.28591

Correspondence to - John F. Thompson - john.thompson@melanoma.org.au

Video short - https://www.youtube.com/watch?v=1rOlvR5_6Sg

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Keywords - cancer, melanoma, metastasis, time, adjuvant systemic therapy, tumor doubling time

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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When Does a Melanoma Metastasize? Implications for Management

BUFFALO, NY - August 7, 2024 – A new #editorial paper was #published in Oncotarget's Volume 15 on July 12, 2024, entitled, “How to deal with runaway metastatic disease?”

In this new editorial, Justine Paris and Guilhem Bousquet from Université Paris Cité, Université Sorbonne Paris Nord, and APHP, Hôpital Avicenne, Oncologie médical, discussed how their research team have shown that PROM2 is a predictive biomarker of distant metastases and shorter survival among patients with stage III melanomas. 

More recently, in a large preclinical study using cancer cell lines and various mouse models of human melanomas, the researchers also demonstrated that the runaway metastatic process is closely linked to PROM2 overexpression, through the increase of epithelial-to-mesenchymal transition (EMT) marker expression and ferroptosis resistance. 

“We report two critical findings: (i) these findings, initially observed in melanoma, have also been confirmed in renal and breast cancers; (ii) we successfully implemented an original in vivo model of metastatic runaway in order to mimic what occurs in patients.”

DOI - https://doi.org/10.18632/oncotarget.28609

Correspondence to - Guilhem Bousquet - guilhem.bousquet@aphp.fr

Video short - https://www.youtube.com/watch?v=PQr3Hb97Brw

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Keywords - cancer, metastatic disease, PROM2, biomarker, tumor growth models

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Dealing with Runaway Metastatic Disease

BUFFALO, NY- August 15, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on August 14, 2024, entitled, “A nanobody against the V-ATPase c subunit inhibits metastasis of 4T1-12B breast tumor cells to lung in mice.”

The vacuolar H+-ATPase (V-ATPase) is an ATP-dependent proton pump that functions to control the pH of intracellular compartments as well as to transport protons across the plasma membrane of various cell types, including cancer cells.  

Researchers Zhen Li, Mohammed A. Alshagawi, Rebecca A. Oot, Mariam K. Alamoudi, Kevin Su, Wenhui Li, Michael P. Collins, Stephan Wilkens, and Michael Forgac from Tufts University School of Medicine; Tufts University; Dana Farber Cancer Institute, Harvard Medical School; University of Minnesota School of Medicine; Prince Sattam Bin Abdulaziz University; Korro Bio; SUNY Upstate Medical University; and Foghorn Therapeutics, have previously shown that selective inhibition of plasma membrane V-ATPases in breast tumor cells inhibits the invasion of these cells in vitro. They have now developed a nanobody directed against an extracellular epitope of the mouse V-ATPase c subunit.

“We show that treatment of 4T1-12B mouse breast cancer cells with this nanobody inhibits V-ATPase-dependent acidification of the media and invasion of these cells in vitro.”

The research team further found that injecting this nanobody into mice implanted with 4T1-12B cells orthotopically in the mammary fat pad inhibited the metastasis of tumor cells to the lungs.

“In conclusion, our results indicate that a nanobody directed against an extracellular epitope expressed on the surface of the V-ATPase is able to inhibit activity of cell surface V-ATPases in 4T1-12B breast cancer cells, inhibit in vitro invasion of these cells and inhibit metastasis of these cells to lung following their implantation in the mammary fat pad of mice.”

DOI - https://doi.org/10.18632/oncotarget.28638

Correspondence to - Michael Forgac - michael.forgac@tufts.edu

Video short - https://www.youtube.com/watch?v=4eLGqvSfAgg

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Keywords - cancer, vacuolar ATPase, breast cancer, invasion, tumor metastasis, tumor growth

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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Nanobody Inhibits Metastasis of Breast Tumor Cells to Lung in Mice

BUFFALO, NY- August 28, 2024 – A new #research paper was #published in Oncotarget's Volume 15 on August 26, 2024, entitled, “Inhibition of miR-10b treats metastatic breast cancer by targeting stem cell-like properties.”

As stated within the Abstract of the paper, despite advances in breast cancer screening and treatment, the prognosis for metastatic disease remains dismal, with only a 30% five-year survival rate. This poor outcome is largely due to the failure of current therapeutics to target the unique properties of metastatic cells. One of the key drivers of metastasis is miR-10b, a small noncoding RNA implicated in cancer cell invasion, migration, viability, and proliferation. 

Researchers Alan Halim, Nasreen Al-Qadi, Elizabeth Kenyon, Kayla N. Conner, Sujan Kumar Mondal, Zdravka Medarova, and Anna Moore from Michigan State University’s Precision Health Program, College of Human Medicine, and College of Veterinary Medicine, and Transcode Therapeutics Inc. in Newton, Massachusetts, provide transcriptional evidence that inhibiting miR-10b with MN-anti-miR10b—a nanodrug designed to deliver anti-miR-10b antisense oligomers to cancer cells—activates developmental processes in cancer cells. They observed increased miR-10b expression in stem-like cancer cells.

In mouse models of metastatic triple-negative breast cancer, MN-anti-miR10b has been shown to prevent the onset of metastasis and eliminate existing metastases when combined with chemotherapy, even after treatment has been discontinued.

"Our results demonstrate that inhibition of miR-10b using MN-anti-miR10b decreases the stemness of breast cancer cells, supporting dedifferentiation as a mechanism through which the nanodrug may function as a therapy."

DOI - https://doi.org/10.18632/oncotarget.28641

Correspondence to - Anna Moore - moorea57@msu.edu

Video short - https://www.youtube.com/watch?v=BtaZd_iV8dI

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Keywords - cancer, breast cancer, metastasis, stem-like cells, nanoparticle, miR-10b

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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miR-10b Inhibition: A Strategy for Treating Metastatic Breast Cancer

While there have been significant improvements in breast cancer detection and treatment, the outlook for metastatic breast cancer remains bleak, with only a 30% five-year survival rate. This is largely due to existing therapies’ inability to effectively target the unique characteristics of metastatic cells. One key factor in metastasis is miR-10b, a small noncoding RNA known to influence cancer cell invasion, migration, viability, and proliferation.

In their paper, researchers Alan Halim, Nasreen Al-Qadi, Elizabeth Kenyon, Kayla N. Conner, Sujan Kumar Mondal, Zdravka Medarova, and Anna Moore from Michigan State University’s Precision Health Program, College of Human Medicine, and College of Veterinary Medicine, and Transcode Therapeutics Inc. in Newton, Massachusetts, shared findings showing that inhibiting miR-10b impairs breast cancer cell stemness. Their research paper, entitled, “Inhibition of miR-10b treats metastatic breast cancer by targeting stem cell-like properties” was published in Volume 15 of Oncotarget on August 26, 2024.

Full blog - https://www.oncotarget.org/2024/10/11/targeting-stem-cell-like-traits-how-mir-10b-inhibition-treats-metastatic-breast-cancer/

Research DOI - https://doi.org/10.18632/oncotarget.28641

Correspondence to - Anna Moore - moorea57@msu.edu

Video short - https://www.youtube.com/watch?v=BtaZd_iV8dI

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Keywords - cancer, breast cancer, metastasis, stem-like cells, nanoparticle, miR-10b

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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Targeting Stem Cell-like Traits: How miR-10b Inhibition Treats Metastatic Breast Cancer

BUFFALO, NY - November 4, 2024 – A new #casereport was #published in Oncotarget's Volume 15 on October 11, 2024, entitled “A case of adenosquamous pancreatic cancer with a KRAS G12C mutation with an exceptional response to immunotherapy.”

This case report highlights a remarkable and unexpected response to immunotherapy in a patient with metastatic adenosquamous pancreatic cancer (ASCP), a rare and aggressive form of pancreatic cancer. The study, led by Murtaza Ahmed, Brent K. Larson, Arsen Osipov, Nilofer Azad, and Andrew Hendifar from Cedars-Sinai Medical Center and Johns Hopkins University, provides new hope for ASCP patients, who are traditionally underserved by current treatment options.

The team documented a 68-year-old male with metastatic ASCP carrying a KRAS G12C mutation. Unexpectedly, after limited success with standard therapies, the patient’s cancer responded significantly to pembrolizumab, a type of immune checkpoint inhibitor, despite the absence of typical markers indicating suitability for immunotherapy.

Pancreatic cancer remains one of the most lethal cancer types, with few advancements in effective treatments for its rarer forms, such as ASCP, which accounts for only 1-10% of all pancreatic cancer cases. Traditionally, ASCP has been treated with chemotherapy based on protocols for the more common pancreatic ductal adenocarcinoma, despite the distinct tumor characteristics. 

This case suggests that ASCP’s unique tumor microenvironment may make it more receptive to immunotherapy. Researchers are hopeful that this new understanding will drive clinical trials focused on immunotherapy specifically for ASCP patients, potentially offering new options for those with limited treatment success. 

“To that point, there is an active multi-center phase 2 trial investigating outcomes and responses to ICI in patients with metastatic or unresectable ASCP or ampullary cancer.” 

In conclusion, this report signals a potential shift in the treatment of rare and aggressive pancreatic cancer subtypes like ASCP. As oncology increasingly embraces personalized medicine, cases like this one open new avenues for patients who were not responsive to traditional therapies, potentially transforming the management of previously intractable cancers.

DOI - https://doi.org/10.18632/oncotarget.28659

Correspondence to - Andrew Hendifar - andrew.hendifar@cshs.org

Video short - https://www.youtube.com/watch?v=VnfohGvfMoM

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Keywords - cancer, pancreatic cancer, immunotherapy, metastasis

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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Immunotherapy Success in KRAS G12C Adenosquamous Pancreatic Cancer

Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Oncotarget is now indexed by MEDLINE, PubMed and PMC/PubMed.

Read about the Oncotarget Scientific Integrity Process: https://www.oncotarget.com/scientific_integrity/

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