Cervical cancer is one of the malignant tumors with high incidence and high mortality among women in developing countries. The main factors affecting the prognosis of cervical cancer are the late recurrence and metastasis and the effective adjuvant treatment, which is radiation and chemotherapy or combination therapy. Galectins, a family containing many carbohydrate binding proteins, are closely involved in the occurrence and development of tumor. They are involved in tumor cells transformation, angiogenesis, metastasis, immune escape, and sensitivity against radiation and chemotherapy. Therefore, galectins are deemed as the targets of multifunctional cancer treatment. In this review, we mainly focus on the role of galectins, especially galectin-1, galectin-3, galectin-7, and galectin-9 in cervical cancer, and provide theoretical basis for potential targeted treatment of cervical cancer.

Concurrent radio chemotherapy treatment prolongs the survival rate of patients with advanced cervical cancer; however, it has adverse side‑effects. β‑elemene, an active component of the traditional Chinese medicinal herb Curcuma zedoaria, is a promising alternative therapeutic drug for the treatment of advanced cervical cancer. The aim of the present study was to investigate the antitumor effects of β‑elemene in human cervical cancer SiHa cells and to determine its underlying therapeutic molecular mechanisms. Cell viability, cell cycle progression and apoptosis were detected using an MTT assay and flow cytometry analysis. Furthermore, the levels of cell migration and cell invasion were investigated using Transwell and wound healing assays. The expression levels of Cyclin‑dependent kinase inhibitor 2B (P15), Cyclin D1, cellular tumor antigen p53, apoptosis regulator Bcl‑2 (Bcl‑2), apoptosis regulator BAX (Bax), 72 kDa type IV collagenase (MMP‑2), matrix metalloproteinase‑9 (MMP‑9), β‑catenin, transcription factor 7 (TCF7), and Myc proto‑oncogene protein (c‑Myc) were analyzed via western blotting. The results revealed that β‑elemene inhibited the proliferation of SiHa cells in a dose and time‑dependent manner. Administration of β‑elemene induced G1 phase cell‑cycle arrest, as demonstrated by the upregulation of P15 expression and the downregulation of Cyclin D1 expression. Furthermore, the present study revealed that β‑elemene induced apoptosis in SiHa cells by enhancing the expression of p53 and Bax, and suppressing the expression of Bcl‑2. In addition, treatment with β‑elemene inhibited cell migration and invasion via downregulation of MMP‑2 and MMP‑9 expression levels. Western blotting demonstrated that β‑elemene reduced the expression levels of β‑catenin and its downstream target molecule TCF7, thus resulting in reduced levels of their target proteins, including c‑Myc, Cyclin D1, Bax and MMP‑2 in cervical cancer cells. The results of the present study suggested that β‑elemene may inhibit cell proliferation and invasion, in addition to inducing apoptosis, via attenuation of the Wnt/β‑catenin signaling pathway in cervical cancer cells.

Numerous studies have revealed that cofilin-l (CFL1) is associated with cancer cell migration and invasion in various types of tumor tissues. We investigated the roles of CFL1 in vulvar squamous cell carcinoma (VSCC). CFL1 expression was detected in VSCC and normal vulvar tissues using immunohistochemistry and western blotting. The vulvar carcinoma SW962 cell line was transfected with CFL1 small interfering RNA (siRNA) and exposed to periplocoside. We then assessed changes in cell proliferation, apoptosis, invasion and metastasis. We detected changes in CFL1 mRNA and protein expression by RT-PCR and western blotting, and alterations in protein expression of various relevant molecules by western blotting. CFL1 expression was found to be significantly upregulated in the VSCC tissues compared with the normal vulvar tissues by immunohistochemistry and western blotting (P<0.05) and was positively correlated with International Federation of Gynecology and Obstetrics (FIGO) stage, differentiation and lymphatic metastasis (P<0.05). After CFL1 knockdown by siRNA transfection, SW962 cells exhibited a decrease in growth, G1 phase cell cycle arrest, induction of apoptotic, low invasion and metastasis, and disrupted lamellipodium formation. We found that the protein expression of Bcl-xL, cyclin A1, MMP2, MMP9 and STAT3 was decreased, while expression of Bax was increased. Periplocoside inhibited SW962 cell growth, promoted apoptosis, suppressed invasion and migration, and lamellipodium formation. Periplocoside exposure resulted in lower CFL1, Bcl-xL, cyclin A1, MMP2, MMP9 and STAT3 levels, but a higher Bax level compared with the control group. We demonstrated that abnormal CFL1 expression may affect vulvar carcinogenesis and subsequent progression. CFL1 silencing by siRNA significantly inhibited VSCC cell progression, which suggests that CFL1 is a potential therapeutic target for vulvar cancer. Periplocoside, which was utilized in the present study for the clinical treatment of vulvar cancer, showed strong antitumor effects by suppression of CFL1 expression.

Lichen sclerosus is a chronic and inflammatory disease. Extensive studies have focused on the epidermis, with the dermis or epidermis‑dermis receiving less attention. To investigate the role of galectin‑7, a keratinocyte protein, in vulvar lichen sclerosus (VLS) and its potential effects on dermal fibroblasts, immunohistochemical staining was performed with VLS tissue samples and normal control samples. The expression of galectin‑7 was determined by evaluating the galectin‑7 integrated density analysis, and further assessed by western blot analysis. Dermal fibroblasts were isolated from the normal tissue of the female anogenital region following sexual plastic surgery. A cell viability assay was performed on isolated dermal fibroblast cells in the presence or absence of galectin‑7. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was performed to determine the transcriptional level of collagen I and collagen III in the response to different doses of galectin‑7. In the immunohistochemical analysis, galectin‑7 demonstrated a significantly elevated level in VLS, compared to control tissues, which was confirmed by western blot analysis. In the analysis of primary dermal fibroblast cells, galectin‑7 significantly inhibited the viability rate of fibroblasts in a dose‑dependent manner. RT‑qPCR data revealed that the transcription level of collagen I and collagen III were positively associated with the galectin‑7 treatment concentration. The overexpression of galectin‑7 is associated with the progression of VLS in the epidermis, a high concentration of galectin‑7 inhibits the viability of the primary vulvar dermal fibroblasts, and stimulates the accumulation of collagen I and collagen III in dermal fibroblast cultures, thus galectin‑7 may serve as a drug target during VLS progression.