Fig 2: The high expression of ARP2 and ARP3 is associated with a poor prognosis of Cervical Squamous Cell Carcinoma. (A,B) Box plot of expression of ARP2 and ARP3 in CSCC. Gene expression analysis and survival analysis were performed by the GEPIA database. (C,D) The survival analysis of ARP2 and ARP3 in CSCC. Gene expression analysis and survival analysis were performed by the GEPIA database.

Fig 3: ARP3 localized on microfilaments and Lipid droplets (LDs). (A) Subcellular localization of ARP3 and LDs, bar, 10 µm. Arrow:co-location between LDs, Arp3, and microfilaments. (B) The binding of artificial LDs (aLDs) or intracellular LDs (cLDs) and actin, bar, 10 µm. (C) The binding of isolated intracellular LDs (cLDs) and actin after being treated with siNC or siARP3, bar, 4 µm. (D) The Quantitative Analysis of LDs binding with microfilaments of (B), ** p < 0.01. (E) The Quantitative Analysis of LDs binding with microfilaments of (C), ** p < 0.01. (F) Schematic diagram of ARP3 truncation fragments. (G) Subcellular localization of ARP3 truncation fragments and microfilament, bar, 5 µm. (H) Subcellular localization of ARP3 truncation fragments and LDs, bar, 5 µm.

Fig 4: ARP2 and ARP3 regulate the expression level of FA and lipid synthesis-related genes. (A) Interference efficiency detection by qRT-PCR. * p < 0.05, ** p < 0.01 (B) The expression level of fatty acid synthesis-related genes detected by qRT-PCR. * p < 0.05. (C) The expression level of lipid synthesis-related genes detected by qRT-PCR. * p < 0.05. (D) Overexpression efficiency detection by qRT-PCR. ** p < 0.01. (E) The expression level of fatty acid synthesis-related genes detected by qRT-PCR. * p < 0.05. (F) The expression level of lipid synthesis-related genes detected by qRT-PCR. * p < 0.05. (G) The ASK1-p38-JNK and AKT signaling in groups of interfered ARP3 and control cells as detected by Western Blot experiments. (H) The ASK1-p38-JNK and AKT signaling in the overexpression cell group and control cells as detected by Western Blot experiments. (I) A grey value analysis of G. ImageJ software (ImageJ 1.52a, NIH, Bethesda, MD, USA)was used for this analysis, according to the instructions. * p < 0.05, ** p < 0.01. (J) A grey value analysis of H. ImageJ software (ImageJ 1.52a, NIH, Bethesda, MD, USA)was used for this analysis, according to the instructions. * p < 0.05, ** p < 0.01.

Fig 5: MYH9 regulates LD content. (A) The expression of MYH9 of isolated cLDs after interfering with ARP3 and control cells was detected by Western Blot experiments. (B) Detection of the cellular LDs marked by BODIPY493/503 through a laser scanning confocal microscope. The Hela cells were transfected with siNC or siMYH9 for 48 h. Subsequently, the cells were treated with 400 µM oleic acid for another 6 h. Then, the cells were fixed and stained for observation by microscope. bar, 10 µm. (C,D) The gray value analysis of the difference in the number of LDs. * p < 0.05, ** p < 0.01. (E,F) Analysis of the difference in the content of triglycerides and hydrolysis rate after interference MYH9. * p < 0.05, ** p < 0.01. (G) Detection of the interaction of LDs and mitochondrion after siMYH9. ** p < 0.01.