RhoC is a G protein present in some cancers. RhoC is an RNA sequence that facilitates the assembly of focal adhesions and the organization of actin stress fibers. It is related to other genes within the Rho family which regulates cell motility. RhoC is commonly expressed in whole blood cells, pancreatic tissues, and breast tissues. Our null hypothesis was that RhoC suppresses and regulates cancer cells. This is very significant in order to design drugs to decrease tumor metastasis and to inhibit several mutations if it is a common mutation, as well as, for individuals with cancer affected by the mutations of RhoC. It is also important because the frequency percentage of the mutation is extremely low that allows us to conclude this is not a driver mutation. Within a cell this G protein is most commonly located on the cytoplasmic side of the cell in the cell membrane or lipid-anchor. However, in some cases RhoC can be found in the cleavage furrow if the cell is dividing. This could mean RhoC has a role in regulation during cytokinesis which makes tumors become malignant. When RhoC is overexpressed, it enhances metastasis which means this is an important regulator in tumor invasion (Clark, Golub, Lander, & Hynes, 2000). A study on breast cells found metastasis is part of what makes Inflammatory Breast Cancer so aggressive in the beginning stages. They concluded in this study that overexpression directly impacted angiogenic factors of cancer cells. Researchers found over 90% of tumor samples had overexpressed RhoC within them(Golen, Wu, Qiao, Bao, & Merajver, 2000). Since RhoC is a key regulator for cancer stem cells a study was performed to see the effects of RhoC on ovarian cancer cells. A PCR was run to observe the expression levels of RhoC along with other proteins. It was concluded that si-RhoC suppressed expression levels of the other proteins, drug resistance and invasion (Sang et al., 2016). RhoC is commonly experimented with how it can regulate specific cancer cells. Another research team studied the effects of RhoA and RhoC on prostate cancer cells. This team specifically tested its effects on glutamine metabolism that is a contributor to cell growth in prostate cancer. They concluded that RhoC overexpression did not show a specific impact to the lack of glutamine. Although the dominant negative mutation of the RhoC protein was more resistant than the overexpressed RhoC (Paiva et al., 2018)
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