Related Experiment Video
Updated: Jan 20, 2026
Competing-Risk Nomogram for Predicting Cancer-Specific Survival in Multiple Primary Colorectal Cancer Patients after Surgery
Published on: September 27, 2024
Sam68 is required for the growth and survival of nonmelanoma skin cancer
Kai Fu1,2,3, Xin Sun3,4, Xue Xia3
1Institute of Molecular Precision Medicine and Hunan Key Laboratory of Molecular Precision Medicine, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Abstract:
Although targeting DNA repair signaling pathways has emerged as a promising therapeutic for skin cancer, the relevance of DNA damage responses (DDR) in the development and survival of nonmelanoma skin cancer (NMSC), the most common type of skin cancer, remains obscure. Here, we report that Src-associated substrate during mitosis of 68 kDa (Sam68), an early signaling molecule in DDR, is elevated in skin tumor tissues derived from NMSC patients and skin lesions from Gli2-transgenic mice. Downregulation of Sam68 impacts the growth and survival of human tumor keratinocytes and genetic ablation of Sam68 delays the onset of basal cell carcinomas (BCC) in Gli2-transgenic mice. Moreover, Sam68 plays a critical role in DNA damage-induced DNA repair and nuclear factor kappa B (NF-κB) signaling pathways in keratinocytes, hence conferring keratinocyte sensitivity to DNA damaging agents. Together, our data reveal a novel function of Sam68 in regulating DDR in keratinocytes that is crucial for the growth and survival of NMSC.
Insights
Src-associated substrate during mitosis of 68 kDa (Sam68) is crucial for nonmelanoma skin cancer (NMSC) growth. This study reveals Sam68’s role in DNA damage response, impacting skin cancer development and survival.
Area of Science:
- Oncology
- Molecular Biology
- Dermatology
Background:
- Targeting DNA repair signaling pathways is a promising strategy for skin cancer therapy.
- The role of DNA damage responses (DDR) in nonmelanoma skin cancer (NMSC) development and survival is not well understood.
Purpose of the Study:
- To investigate the role of Src-associated substrate during mitosis of 68 kDa (Sam68) in NMSC.
- To elucidate Sam68's function in DNA damage response pathways within keratinocytes.
Main Methods:
- Quantification of Sam68 expression in NMSC patient tissues and Gli2-transgenic mouse models.
- Assessment of Sam68's impact on keratinocyte proliferation and survival.
- Evaluation of Sam68's role in DNA repair and NF-κB signaling following DNA damage.
- Genetic ablation of Sam68 in Gli2-transgenic mice to observe effects on basal cell carcinoma (BCC) development.
Main Results:
- Sam68 is upregulated in NMSC tissues and skin lesions from Gli2-transgenic mice.
- Downregulation of Sam68 inhibits human tumor keratinocyte growth and survival.
- Genetic ablation of Sam68 delays BCC onset in Gli2-transgenic mice.
- Sam68 is essential for DNA damage-induced DNA repair and NF-κB signaling in keratinocytes.
Conclusions:
- Sam68 is a novel regulator of DNA damage response in keratinocytes.
- Sam68 plays a critical role in the growth and survival of NMSC.
- Targeting Sam68 may represent a potential therapeutic strategy for NMSC.
Related Concept Videos
01:29Oxygen Requirements and Growth Patterns
01:21Cancer Survival Analysis
01:30Skin Cancer
Basal Cell Carcinoma (BCC): BCC is the most common type of skin cancer, accounting for about 80% of cases. It typically develops in...
01:20Accessory Structures of the Skin: Hair Growth and Types
01:26Requirements for Human Life
Oxygen
Atmospheric air is only about 20 percent oxygen, but that oxygen is a key component of the chemical reactions that keep the body alive, including the reactions that produce ATP. Brain cells are susceptible to a lack of oxygen because they require a...
01:19Survival Tree
Building a Survival Tree
Constructing a...