Related Experiment Video
Updated: Aug 24, 2025
Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
GLDC mitigated by miR-30e regulates cell proliferation and tumor immune infiltration in TNBC
Huaying Xie1, Tingting Yan2, Xinxin Lu3
1Department of Radiation Oncology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Background:
TNBC, whose clinical prognosis is poorer than other subgroups of breast cancer, is a malignant tumor characterized by lack of estrogen receptors, progesterone hormone receptors, and HER2 overexpression. Due to the lack of specific targeted drugs, it is crucial to identify critical factors involved in regulating the progression of TNBC.
Methods:
We analyzed the expression profiles of TNBC in TCGA and the prognoses values of GLDC. Correlations of GLDC and tumor immune infiltration were also identified. CCK8 and BrdU incorporation assays were utilized to determine cell proliferation. The mRNA and protein levels were examined by using Real-time PCR and Western blot analysis.
Results:
In the present study, we analyzed the mRNA expression profiles of TNBC in TCGA and found that GLDC, a key enzyme in glycine cleavage system, was significantly up-regulated in TNBC tissues and higher expression of GLDC was correlated with a worse prognosis in TNBC. Moreover, the expression of GLDC was negatively correlated with macrophage and monocyte and positively correlated with activated CD4 T cell and type 2 T helper cell in TNBC. Overexpression of GLDC facilitated the proliferation of TNBC cells, whereas GLDC knockdown had the opposite effects. Additionally, miR-30e acts as a functional upstream regulator of GLDC and the inhibitory effects of miR-30e on cell proliferation were mitigated by the reintroduction of GLDC.
Conclusions:
These results imply that miR-30e-depressed GLDC acts as a tumor suppressive pathway in TNBC and provides potential targets for the treatment of TNBC.
Insights
Glycine dehydrogenase (GLDC) is upregulated in triple-negative breast cancer (TNBC), promoting tumor growth. Targeting the miR-30e/GLDC pathway may offer new therapeutic strategies for TNBC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Triple-negative breast cancer (TNBC) presents a poorer clinical prognosis compared to other breast cancer subtypes.
- TNBC is characterized by the absence of estrogen receptors, progesterone receptors, and HER2 overexpression.
- The lack of specific targeted therapies underscores the need to identify key regulators of TNBC progression.
Purpose of the Study:
- To investigate the role of Glycine Dehydrogenase (GLDC) in triple-negative breast cancer (TNBC).
- To explore the correlation between GLDC expression, patient prognosis, and tumor immune infiltration in TNBC.
- To elucidate the regulatory relationship between miR-30e and GLDC in TNBC cell proliferation.
Main Methods:
- Analysis of TNBC mRNA expression profiles from The Cancer Genome Atlas (TCGA).
- Assessment of GLDC expression and its correlation with prognosis and immune cell infiltration.
- In vitro assays including CCK8, BrdU incorporation, Real-time PCR, and Western blot to evaluate cell proliferation and molecular changes.
Main Results:
- GLDC was significantly upregulated in TNBC tissues and associated with worse prognosis.
- GLDC expression inversely correlated with macrophages and monocytes, but positively with activated CD4 T cells and type 2 T helper cells.
- GLDC overexpression enhanced TNBC cell proliferation, while knockdown inhibited it; miR-30e acts as an upstream regulator of GLDC.
Conclusions:
- The miR-30e-mediated downregulation of GLDC functions as a tumor-suppressive pathway in TNBC.
- GLDC and its regulatory pathway represent potential therapeutic targets for TNBC treatment.
