Effect of glaucocalyxin B on the protein expressions of PTEN, Beclin1 and LC3 in a mouse model of transplanted cervical cancer, and its significance

  • Zheng Zhao
  • Zhengyang Han
  • Cong Huang
  • Feixiang Yang
Keywords: Glaucocalyxin B, Mouse, Cervical cancer transplanted tumor, PTEN, Beclin1, LC3

Abstract

Purpose: To determine the effect of glaucocalyxin B (GLB) on the protein expressions of PTEN, Beclin1 and LC3 in a mouse model of transplanted cervical cancer, and its significance.
Methods: A mouse model of transplanted cervical cancer was established in female BALB/C mice. The model mice were divided into control group, low-dose GLB group and high-dose GLB group. Mice in low-dose and high-dose groups were given intraperitoneal injection of low-dose GLB and high-dose GLB, respectively. The volume and weight of transplanted tumor were measured and compared between the two groups. Serum levels of CEA and CA125 were assayed by enzyme-linked immunosorbent assay (ELISA). The expressions of phosphatase and tensin homolog (PTEN), autophagy-related factor microtubule-associated protein-1 (Beclin-1), microtubule-associated protein 1 light chain 3 (LC3), apoptosis-related protein p53, and Bax were determined using SABC immunohistochemical operation.
Results: On days 5, 10 and 15, the volume and weight of transplanted tumor, and levels of CA125 and CEA in low- and high-dose GLB groups were significantly and dose-dependently lower than those in control group (p < 0.05). Results from immunohistochemistry showed that the protein expression levels of PTEN, Beclin-1, LC3, p53 and Bax were significantly and dose-dependently higher in low- and highdose GLB groups than in the control group (p < 0.05).
Conclusion: Glaucocalyxin B significantly and dose-dependently induces apoptosis of cervical cancer cells and inhibits their growth by regulating the protein expressions of PTEN, Beclin1 and LC3. Thus, glaucocalyxin B is a potential adjunct therapy in the management of cervical cancer.

Published
2022-06-17
Section
Articles

Journal Identifiers


eISSN: 1596-9827
print ISSN: 1596-5996