Momordicae Semen inhibits migration and induces apoptotic cell death by regulating c-Myc and CNOT2 in human pancreatic cancer cells

Sep 24, 2026

Pancreatic cancer has poor prognosis, and limited chemotherapy response motivates identification of new targets and anticancer agents. This study evaluates whether Momordicae Semen (MS) extract suppresses pancreatic cancer by modulating c-Myc through CNOT2. Cell viability, proliferation, apoptosis, and migration were assessed using MTT, colony formation, immunoblotting, immunofluorescence, and wound healing assays, alongside LC-MS profiling of methanol extract composition. MS regulated apoptotic factors, destabilized c-Myc, and increased apoptosis, while enhancing 5-FU sensitivity, supporting MS as a promising drug candidate.

LanguageEnglish

CategoryHealthcare

FormatPDF

Pages13

Reading Time33 min

AccessFree to download

Introduction

Pancreatic cancer burden and therapy limitations

c-Myc as an oncogenic driver

CNOT2 and the CCR4-NOT complex in cancer

Rationale for Momordicae Semen

Materials and Methods

Experimental evaluation plan and assay set

Chemical composition analysis

Results

MS extract effects on cancer cell phenotypes

[www. nature.com/scientificreports](www. nature.com/scientificreports) OPEN Momordicae Semen inhibits migration and induces apoptotic cell death by regulating c‑Mycand CNOT2 in human pancreatic cancer cells Wona Jee1,2, Hyun Min Ko1,2, Do‑Il Park1,2, Ye‑Rin Park1,2, So‑Mi Park1,2, Hyungsuk Kim3, Yun‑Cheol Na4, Ji Hoon Jung1,2 & Hyeung‑Jin Jang1,2* Pancreatic cancer(PC) is less common than other cancers; however, it has a poor prognosis. Therefore, studying novel target signaling and anticancer agents is necessary. Momordicae Semen (MS), the seed of Momordica sochinensis Spreng, mainly found in South‑East Asia, including China and Bangladesh, is used to treat various diseases because of its anticancer, antioxidant, anti‑inflammatory, and antibacterial properties. However, the effect ofthe MS extract on pancreatic cancer cells remains unknown. In this study investigated whether the MS extract exerted an anti‑cancer effect by regulating c‑Mycthrough CNOT2. Cytotoxicity and proliferation were investigated using MTT and colony formation assays. The levels of apoptotic, oncogenic, and migration‑associated factors were confirmed using immunoblotting and immunofluorescence. Wound closure was analyzed using a wound healing assay. The chemical composition ofthe MS methanol extracts was analyzed using liquid chromatography–mass spectrometry. We confirmed that the MS extract regulated apoptotic factors and attenuated the stability of c‑Myc and its sensitivity to fetal bovine serum. Furthermore, the MS extract increased apoptosis by regulating c‑Myc andCNOT2 expression and enhanced the sensitivity of 5‑FU in pancreatic cancer. This study showed that the MS extract is a promising new drug for PC. In 2020, pancreatic cancer was the 7th most common cancer in men and women, accounting for 2.6 % of cases and 4.7 % of mortalities from all cancer-causing sites1,2. Additionally, pancreatic cancer is one of the cancers with the worst prognosis because it easily metastasizes to nearby organs or lymph nodes3. Recent studies reported that FOLFIRINOX therapy consists of gemcitabine, capecitabine or folinic acid, fluorouracil, irinotecan, and oxaliplatin is the first-line adjuvant chemotherapy for pancreatic cancer4. Although many studies have been conducted on pancreatic cancer, the response to chemotherapy is limited, and the 5-year survival rate of patients with PC has not improved over the past 30 years. Furthermore, pancreatic cancer is difficult to detect in its early stages and metastasizes quickly; making it challenging to treat through surgery5. Therefore, there is a need to identify novel biomarkers and anticancer agents with clear relevance to pancreatic cancer6. The c-Myc oncogene has been implicated in the pathogenesis of several cancers, including pancreatic, hepatocellular, and breast cancers. c-Myc is a transcription factor that regulates cell life and death, including metabolism, mitochondrial function, ribosome biosynthesis, differentiation, apoptosis, and cancer cell proliferation7–9. In humans, c-Myc, located on chromosome 8, binds to the enhancer box (E-box) to regulate gene expression. Like many other transcription factors, MYC is an unstable protein degraded by ubiquitination, such as the Ub ligase Skp2, which regulates c-Myc stability. c-Myc is also overexpressed in primary pancreatic cancer at a rate of 43.5% . Overexpression of c-Myc induces the conversion of pancreatic intraepithelial neoplasm (PanIN) to pancreatic cancer, and c-Myc inhibition suppresses cell proliferation in PC in vitro and induces chemotherapy 1College of Korean Medicine, Kyung Hee University, 26, Kyungheedae-Ro, Dongdaemun-Gu, Seoul 02447, Korea. 2Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Korea. 3Department of Korean Rehabilitation Medicine, College of Korean Medicine, Kyung Hee University, Seoul, Korea. 4Western Seoul Center, Korea Basic Science Institute, 150 Bugahyeon-Ro, Seodaemun-Gu, Seo

FAQs

What question does the study investigate about Momordicae Semen (MS)?

Whether MS extract exerts anti-cancer effects in human pancreatic cancer cells by regulating c-Myc through CNOT2.

How did the researchers measure anti-cancer effects?

They assessed cytotoxicity and proliferation using MTT and colony formation, evaluated apoptosis-, oncogenic-, and migration-associated factors using immunoblotting and immunofluorescence, and measured migration via wound healing assays.

What key outcomes were confirmed for MS extract?

MS extract regulated apoptotic factors, attenuated c-Myc stability and its sensitivity-related behavior to fetal bovine serum, increased apoptosis via c-Myc and CNOT2 expression changes, and enhanced sensitivity to 5-FU in pancreatic cancer.

Sep 24, 2026

Uploaded by Quinn Holloway