Blocking Key Protein Halts Spread of Cervical Cancer Tumors
Recent research has revealed significant insights into how cervical cancer spreads to lymph nodes, signaling potential new treatments. The study identified a crucial molecule involved in metastasis, aiming to address the challenge of this disease. This work particularly focuses on cervical squamous cell carcinoma, responsible for approximately 80% of cervical cancer cases.
Cervical cancer frequently metastasizes to lymph nodes near the lower spine. Such spread complicates treatment options significantly. According to a study published in Advanced Science, the presence of lymph node metastasis can reduce the five-year survival rate from 95% to 33.3%.
RNA's Role in Cancer Spread
Researchers aimed to discover new drug targets for patients who currently lack treatments aimed at metastasis. They specifically investigated molecules driving lymphatic vessel growth, which facilitates cancer cell spread to lymph nodes. Their key finding was a circular RNA molecule named LNMAC, which stands for lymph node metastasis-associated circular RNA.
Circular RNA shares structural similarities with messenger RNA, akin to that found in COVID-19 vaccines. However, unlike linear messenger RNA, circular RNA forms a loop, providing greater resistance to degradation within cells.
By examining cervical tissue samples, the researchers discovered elevated LNMAC levels in patients with metastatic cervical squamous cell carcinoma, compared to healthy individuals. Increased LNMAC levels corresponded to shorter overall patient survival.
Mechanism of Action and Targeting Metastasis
To further understand LNMAC's role, researchers employed mice to elucidate how LNMAC contributes to lymph node metastasis. Findings indicated that LNMAC influences metastasis via epigenetics, which modify gene activity without altering DNA sequences.
More specifically, LNMAC activates genes encoding the protein FGF2, a growth factor vital for forming new blood and lymphatic vessels. While epigenetic drugs have undergone clinical trials for cancer treatment, their effectiveness has been inconsistent, often resulting in pronounced side effects. Researchers noted that some of these drugs could inadvertently activate genes responsible for FGF2.
Researchers advised caution with these drugs in tumors prone to lymphatic metastasis, especially for cervical squamous cell carcinoma. Instead, they pursued an alternative method: directly targeting and inhibiting FGF2 protein through antibody drugs.
In experimental settings with mice, this approach effectively prevented lymph node metastasis by counteracting LNMAC and impairing new lymphatic vessel formation. The researchers stated the critical role of FGF2 in tumor lymphatic vessel growth may be greater than previously recognized.
Targeting FGF2 may lead to promising treatment options for patients facing metastatic cervical squamous cell carcinoma. However, further tests and eventual clinical trials are necessary to validate these discoveries before they can be utilized for patient benefit. This research could provide renewed hope for many cancer patients lacking effective treatment options.
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