Cancer therapy: switching off oncogenes

Pompetti, Franca; Pilla, Daniela; Giancola, Raffaella

doi:10.1002/bies.10238

Cited by 8 publications

(5 citation statements)

References 22 publications

(21 reference statements)

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“…Our results demonstrate that the upregulation of DNA damage response proteins suggests enhanced DNA repair occurring in PLCD1 overexpressed chondrosarcoma cells. In addition, cell apoptosis detected by flow cytometry analysis suggests the PLCD1 overexpressed chondrosarcoma cells failed to repair DNA damage and caused the programmed cell death [ 22 , 29 ].…”

Section: Discussionmentioning

confidence: 99%

PLCD1-Induced DNA Damage Inhibits the Tumor Growth via Downregulating CDKs in Chondrosarcoma

Shen

Chen

Wang

et al. 2022

Journal of Oncology

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Purpose. Typical genes for the treatment and diagnosis of high-grade chondrosarcoma are still in need. Our study aimed to explore the PLCD1 function in chondrosarcoma for further treatment. Materials and Methods. Our study collected the information of 49 patients in our department. The PLCD1 expression in our cohort was detected and was compared with the TCGA database. PLCD1 knockdown and overexpression cell lines were established stably. Cell viability assay and colony formation assay were performed for cell proliferation. Flow cytometry analysis was performed for cell cycle and apoptosis. Western blotting was performed for PLCD1-related protein expression. Animal xenografts were established to verify the effect of PLCD1 in high-grade chondrosarcoma. Results. Compared with the TCGA database, the relation between PLCD1 expression and the malignancy of chondrosarcoma was demonstrated. A lower PLCD1 expression was detected mainly in high-grade chondrosarcoma. PLCD1 overexpression in high-grade chondrosarcoma suppressed CDKs/cyclins and induced DNA damage causing cell cycle blocking and apoptosis. Antitumor effect of PLCD1 overexpression was verified in vivo. Conclusion. Lower PLCD1 was expressed in high-grade chondrosarcoma. Overexpressed PLCD1-induced DNA damage caused cell cycle blocking and apoptosis in vitro and in vivo. PLCD1 could be a novel target in high-grade chondrosarcoma for further drug development.

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Section: Discussionmentioning

confidence: 99%

PLCD1-Induced DNA Damage Inhibits the Tumor Growth via Downregulating CDKs in Chondrosarcoma

Shen

Chen

Wang

et al. 2022

Journal of Oncology

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“…Such an interruption in the progression of the program of oncogenesis might prevent the inevitable march of gene activations. 25 …”

Section: Program Selection and Oncogene Additionmentioning

confidence: 97%

Colorectal cancer prevention

Kauh

Umbreit

2004

Current Problems in Cancer

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“…This monoclonal antibody was found to be effective in 35% of the breast cancer patients who have ErbB2 amplification [146]. In addition, in targeted therapy, oncogenes can be silenced with microRNA or RNAi; tumor suppressor genes can be forcefully expressed in cancer cells by adenoviruses [147]. For example, mutations of p53 gene are found in more than 50% of the human cancers, restoration of p53 activity has been used as a treatment strategy.…”

Section: Targeted Cancer Therapymentioning

confidence: 98%

Bone Morphogenetic Protein-Smad Pathway as Drug Targets for Osteoporosis and Cancer Therapy

2008

EMIDDT

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Bone morphogenetic proteins (BMPs) are members of the TGF-beta superfamily. Engaging of BMPs to BMP receptors on the cell surface leads to activation of the receptor kinase activity, which phosphorylates Smad1/5/8. Smad1, 5, or 8, with Smad4, forms a complex, which is translocated to the nucleus, where it binds to the consensus DNA sequence to regulate the transcription of BMP target genes. BMP-Smad signaling regulates stem cell renewal, cell proliferation, differentiation, migration, and apoptosis, and controls embryo development and postnatal tissue homoeostasis. Both human and mouse genetic studies have demonstrated that BMPs play positive roles in postnatal bone homeostasis including osteoblast expansion, differentiation, and bone formation. Defects in BMP-Smad signaling cause bone-related disorders such as osteoporosis, a disease that affects hundreds of millions of people. In addition, BMP-Smad signaling has been shown to play an important role in tumorigenesis. Mounting evidence indicates that in many tissues, BMP-Smad signaling has a tumor-suppressing activity and that BMPs can repress tumor growth. These findings suggest that BMP-Smad pathway can be a potential target not only for osteoporosis therapy but also for cancer therapy.

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Cancer therapy: switching off oncogenes

Cited by 8 publications

References 22 publications

PLCD1-Induced DNA Damage Inhibits the Tumor Growth via Downregulating CDKs in Chondrosarcoma

PLCD1-Induced DNA Damage Inhibits the Tumor Growth via Downregulating CDKs in Chondrosarcoma

Colorectal cancer prevention

Bone Morphogenetic Protein-Smad Pathway as Drug Targets for Osteoporosis and Cancer Therapy

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