Research Roundup: cancer research
Our new Research Roundup summarises three cancer research studies that have used polyclonal antibodies from Atlas Antibodies. Today we share insights into a new biomarker for glioma, the metastatic process in colorectal cancer, and the effect of ginseng metabolites on cancer cells proliferation. Learn more!
1) Tenascin-C expression contributes to pediatric brainstem glioma tumor phenotype and represents a novel biomarker of disease (Qi et al, 2019).
Genes specifically expressed by tumor cells, like tenascin C (TNC), can shape the brain parenchyma. TNC increases the stiffness of the extracellular matrix, which compromises vascular integrity and induces hypoxia. In addition, TNC promotes glioma invasion and angiogenesis resulting in tumor progression and poor prognosis.
In most healthy adult brains, TNC is undetectable but rapidly induced by pro-inflammatory cytokines in various pathological conditions, including gliomas.
Using our anti-TNC (HPA004823) polyclonal antibody, this study analyzed TNC expression on a large cohort of pediatric glioma tissue specimens. The results show that TNC overexpression is also clinically detectable in pediatric high-grade and diffuse midline pontine glioma (DIPG) and may significantly contribute to tumor biology.
TNC endogenous expression levels in pediatric glioma tissue are grade-dependent but higher in tumors harboring the H3K27 M mutation. In conclusion, TNC may contribute to DIPG tumor phenotype and serve as a clinically detectable biomarker for tumor progression.
Figure 1. Tenascin-C is overexpressed in pediatric glioma tissue. IHC staining is stronger in high-grade and midline glioma tissue, compared to low-grade glioma and normal brainstem tissue. Anti-TNC (HPA004823) polyclonal antibody. Image from Qi et al, 2019.
2. Expression of CIB1 correlates with colorectal liver metastases but not with peritoneal carcinomatosis (Jacob et al., 2021).
Molecular differences in colorectal cancer (CRC) are associated with the metastatic route. Patients with CRC might develop metastases either to the liver, the brain, the lungs, or the peritoneum; however, there are also patients who will not metastasize.
Patient survival is mainly driven by metastatic spread thus, it is imperative to understand its key drivers to develop biomarkers for risk stratification, follow-up protocols, and personalized therapy.
Overexpression of the calcium and integrin binding 1 protein (CIB1) is well known in CRC and is associated with deteriorated survival rates. By using our Anti-CIB1 rabbit polyclonal antibody, this study aimed to identify genes associated with the metastatic route in CRC.
Gene expression analysis and immunohistochemical validation revealed a significant correlation of increased CIB1 expression levels with liver metastases, as shown in figure 2 below. Moreover, in future studies, CIB1 might identify patients at risk for metachronous liver metastases.
Figure 2. Immunohistochemical staining of CIB1: Colonic adenocarcinoma with absent (A), weak (B), moderate (C), and strong (D) CIB1 staining (magnification 200-fold). Anti-CIB1 (HPA042413) polyclonal antibody. Image from Jacob et al., 2021.
3. Ginsenoside Rg1 suppresses cancer cell proliferation through perturbing mitotic progression (Hong et al., 2021).
The chromosomal instability resulting from dysregulated mitotic processes is usually increased in cancer.
Ginsenosides, isolated from ginseng, possess medicinal properties owing to their steroidal structure and play major pharmacological roles in various biological processes. Among 150 different types of ginsenosides, Rb1 and Rg1 are the most abundant and responsible for the pharmacological properties of ginseng.
Since the anticancer effect of Rg3 and Rg5 ginsenosides subunits has been previously reported, this study aimed to investigate the anticancer effects of ginsenoside Rg1 on mitotic progression in cancer.
Multiple cancer cell lines were tested: HeLa (uterus adenocarcinoma), MDA-MB-231 (triple-negative breast cancer), MCF7 (luminal A breast cancer), H226B (non-small cell lung carcinoma expressing wild type p53), H226Br (non-small cell lung carcinoma expressing mutant p53), H1299 (p53 deficient non-small cell lung carcinoma), A549 (lung cancer harboring wild type p53), SW480 (colorectal adenocarcinoma), HCT116 (colorectal carcinoma), and RPE1 (immortalized retinal cell) cells.
The results show that ginsenoside Rg1 suppresses cancer cells proliferation only in cervical and triple-negative breast cancer by impeding the mitotic processes, such as chromosome alignment and spindle dynamics,
To better understand the molecular mechanism underlying the genetic background-dependent tumor-suppressive effect of ginsenoside Rg1, the intensity of SGO2 (and other proteins) was analyzed in ginsenoside Rg1-treated cells using our Anti-SGO2 (HPA035163) polyclonal antibody.
Figure 3. Schematic from Hong et al., 2021. Ginsenoside Rg1 reduces the level of Aurora B at the centromere via perturbing Haspin kinase activity and concurrent H3T3ph. Therefore, ginsenoside Rg1 suppresses cancer cell proliferation through impeding mitotic processes, such as chromosome alignment and spindle dynamics, upon depletion of Aurora B from the centromere.
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1. Qi, J., Esfahani, D.R., Huang, T. et al. Tenascin-C expression contributes to pediatric brainstem glioma tumor phenotype and represents a novel biomarker of disease. acta neuropathol commun 7, 75 (2019).