Overexpression of LncRNA SNHG1 Were Suitable for Oncolytic Adenoviruse H101 Therapy in Oral Squamous-Cell Carcinoma

Abstract

Background: As the most prevalent type of head and neck cancer, oral squamous-cell carcinoma (OSCC) accounts for nearly 90% of all oral cancer cases. Despite great progress having been made in the diagnosis and treatment of OSCC recently, the survival rate of OSCC patients has not risen remarkably. Chemotherapy is commonly used for OSCC treatment; however, the emergence of chemoresistance limits its long-term curative effect. Therefore, identifying effective biomarkers and molecular mechanisms is essential to the development of therapeutic strategies for OSCC.

Methods: qRT-PCR assays were performed to detect SNHG1 expression in OSCC tissue and cells, and CCK8 assays and animal experiments used to examine cell proliferation. In addition, CCK8 assays were used to detect IC₅₀ values of cisplatin, 5Fu, Dox, and oncolytic adenovirus H101.

Results: We found that SNHG1 was overexpressed in OSCC tissue and cells and was associated with OSCC progression. In addition, knockdown of SNHG1 suppressed cell proliferation in vitro and in vivo. Importantly, we found that oncolytic adenovirus H101 showed better antitumor effects in OSCC with high SNHG1 expression, and chemotherapy showed worse anti-tumor effects in OSCC with high SNHG1 expression.

Conclusion: SNHG1 can act as a diagnostic biomarker for OSCC, and may be a biomarker for treatment options.

Keywords: H101; OSCC; SNHG1.

Figure 1

SNHG1 was overexpressed in OSCC tissue (n=76.) *p<0.05). All experiments were repeated three times.

Figure 2

Clinical significance of SNHG1 in indicating OSCC progression. (A) Patients with high SNHG1 expression had poor survival. (B) SNHG1 expression had potential clinical significance as a tumor biomarker based on the ROC) curve (n=76).

Figure 3

Knockdown of SNHG1 suppressed cell proliferation in OSCC. (A) The of SNHG1 expression was detected with qRT-PCR assays. (B) Stable knockdown of SNHG1 cells was achieved. CCK8 assays showed knockdown of SNHG1 expression significantly inhibited cell proliferation in SCC25 (C) and HN4 (D) cells. (E) Tumor volume in mice (n=5). (F) Survival ratio in mice. *p<0.05. All experiments were repeated three times.

Figure 4

High SNHG1 expression in OSCC was suitable for H101 therapy. (A) SNHG1 expression was detected with qRT-PCR assays. IC₅₀ of cisplatin (B), Dox (C), 5Fu (D), and H101 (E). *p<0.05. All experiments were repeated three times.