Table 1 Apoptosis-related ncRNAs and colorectal cancer

miRNAs

miR-296-3p

Down

Inhibited

in CRC cells, Circ_0087862 targeted miR-296-3p. The inactivation of miR-296-3p reversed the blockage of cell processes like glycolysis, invasion, reproduction, and apoptosis caused by Circ_0087862

In vivo

[261]

miR133A

Up

Activated

migration, colony formation, and cell viability were potentially decreased, and apoptosis was elevated in CRC cell lines transfected with MIR133A

In vitro

[262]

miR-338-3p

Down

Inhibited

*Circ_0004585 helped CRC cell progression via inhibiting miR-338-3p

* Targeting ZFX inhibited the oncogenic development of CRC cells

In vivo

[263]

miR-652

Up

Activated

In rectal cancer patients, miR-652 expression could be used as a marker to predict radiation response and clinical results

In vitro

[264]

miR-584-5p

Up

Activated

Inhibitory peptides targeted at nucleic acids

In vitro

[265]

miR-425-3p

Up

Activated

Inhibitory peptides targeted at nucleic acids

In vitro

[265]

miR-15b-5p

Down

Inhibited

Decreased metastasis and migration of CR tumor

In vitro

[266,267,268]

miR-138-5p

Down

Inhibited

*Accelerated death of cells but decreased CRC development

*Led to MCU overexpression, in which ROS production was further enhanced to support CRC development

*A decrease in miR-138-5p levels increased mitochondrial biogenesis by targeting MCU, thereby promoting the proliferation of CRC cells. This discovery suggests that miR-138-5p could serve as a potential target for the treatment of CRC

In vitro /

In vivo

[269]

miR-21, miR-31

miR-135a1

Down

Activated

In HCT 116 cells, the water extract from Inula viscosa L. (IVE) showed effects that inhibited cell growth and caused cell death (apoptosis)

In vitro

[270]

miR-145

Up

Activated

In HCT 116 cells, the water extract from Inula viscosa L. (IVE) showed effects that inhibited cell growth and caused cell death (apoptosis)

In vitro

[270]

microRNA-627-5p

Up

Activated

* reduced CRC cells' ability to travel, invade, and continue to exist

* The quantities of RNA (transcript) and protein of the elements involved in the downstream Wnt/-catenin signaling cascade

In vitro

[271]

miR-769-5p

Down

Inhibited

miR-769-5p, providing a new therapeutic target for CRC A brand-new potential therapeutic target for CRC is MiR-769-5p

In vivo

[272]

miR-7-5p

Up

Activated

caused the radiation therapy resistance to be overcome

In vivo

[273]

miR-625-5p

Up

Inhibited

increased cell migration and growth

In vivo

[274]

miR-653

Up

Inhibited

increased development of growth, invasion, and migration

In vitro

[275]

miR-455-3p

Up

Inhibited

increased cell division, reduced cell death, and promoted cell migration

In vivo

[276]

miR-506-3p

Up

Activated

HT29 and SW480 cells' cell cycle, apoptosis, and proliferation were hindered in comparison to control groups

-

[277]

miR-653

Up

Inhibited

*Directly binding to the 3’-UTR of DLD mRNA down-regulated DLD

*The proliferation of cells was increased

In vitro

[278]

miR-486-5p/miR-34c-5p

Up

Activated

Decreased the migration, proliferation, and invasion of malignant cells

In vitro

[279]

microRNA-30c

Up

Activated

The apoptosis rate was measured, and the data showed that apoptosis was triggered in CT-26 cells when they were close to miR-30c-transfected MSCs

In vitro

[280]

miR-378a

Up

Activated

The presence of miR-378a led to a decrease in the growth and mobility of CRC cells. However, when the connection between miR-378a and FOXQ1 and ODC1 was disrupted, the effects of miR-378a were reversed. This indicates that FOXQ1 and ODC1 played a vital role in enabling miR-378a to suppress the growth of CRC cells

In vivo

[281]

miR-200b-3p

Up

Activated

decreased CRC cell invasion, motility, and viability while increased cell death and apoptosis

In vivo

[282]

miR-125b

Up

Activated

In the presence of butyrate, proliferation was reduced, and cell-cycle arrest was increased

In vivo

[283]

miR-181a

Up

Activated

In the presence of butyrate, proliferation was reduced, and cell-cycle arrest was increased

In vivo

[283]

miR-593

Up

Activated

In the presence of butyrate, proliferation was reduced, and cell-cycle arrest was increased

In vivo

[283]

miR-1227

Up

Activated

In the presence of butyrate, proliferation was reduced, and cell-cycle arrest was increased

In vivo

[283]

miR-143-3p

Up

Activated

Extremely was decreased cell proliferation in CRC and pancreatic cancer cell lines by MIR143#12

In vivo

[284]

miR-103a-3p

Down

Activated

In HCT116 and Caco-2 cells, the MiR-103a-3p inhibitor dramatically reduced proliferative potential and induced cell cycle arrest as well as death

In vitro

[104]

miR-144-5p

Up

Activated

RNF187 knockdown decreased CRC cell proliferation, mobility, and attack while boosting apoptosis. RNF187 was also shown to be a direct target of miR-144-5p. RNF187 reduced the development of CRC cells by significantly inhibiting miR-144-5p

In vivo / in vitro

[285]

miR-887-3p

Up

Activated

The microRNA miR-887-3p appears to be a promising biomarker for CRC. It restricts CRC cell proliferation, invasion, and the process of epithelial-mesenchymal transition (EMT). Furthermore, it promotes cell death by targeting and decreasing DNMT1 while increasing P53 expression. As a result, miR-887-3p has the potential to be both a useful biomarker and a therapeutic target in the treatment of CRC

In vivo

[286]

miR-135b

Up

Inhibited

Induced CRC cell proliferation and prevented apoptosis by inhibiting the TGF-signaling pathway

In vitro

[95]

miR-223

Down

Activated

In CRC cells, increasing the levels of miR-223 and decreasing the levels of lipoma preferred partner (LPP) canceled out the tumor-suppressing effects of circLRCH3. Additionally, when miR-223 was reduced, these effects were reversed

In vitro

[96]

miR-17-5p

Up

Inhibited

Encouraging cell growth, movement, and invasion

In vitro

[97]

miR-4449

Down

Activated

CRC cell growth was inhibited

In vivo

[98]

miR-21

Up

Inhibited

Stimulate cell growth, invasion, progression through the cell cycle, and the development of xenografts in mice

In vivo

[99]

miR-126

Up

Activated

MiR-126 overexpression reduced the viability and proliferation of CRC cells. Furthermore, increased expression of miR-126 boosted cell autophagy, as demonstrated by LC3-I/II transformation and p62 degradation

In vivo/ in vitro

[100]

miR-193a-3p

Up

Activated

Through regulation of the PAK3 signaling pathway, it suppressed the viability, cell cycle progression, migration, and invasion of CRC cells in vitro and induced apoptosis

In vitro

[101]

miR-148a

Up

Activated

reduced angiogenesis by directly targeting ROCK1/c-Met and downregulating HIF-1/VEGF and Mcl-1

In vivo/ in vitro

[102]

miR-107

Down

Activated

*MiR-107 was discovered to participate in controlling MCM7 expression through miRNA microarray analysis and 3'UTR reporter assays

*In CRC cells, the significant reduction of MCM7 using shRNA led to a remarkable decrease in cell proliferation, a notable increase in apoptosis in laboratory conditions, and the inhibition of tumor growth in live subjects

In vivo/ in vitro

[103]

miR-296-5p

Down

Activated

Inhibiting miR-103a-3p dramatically reduced the ability of HCT116 and Caco-2 cells to proliferate and resulted in cell cycle arrest, as well as apoptosis

In vitro

[104]

miR-451

Up

Activated

decreased proliferation and migration, increased apoptosis, and boosted the sensitivity of CRC cells to chemotherapy

In vivo/ in vitro

[106]

miR-21

Down

Activated

It may be a valuable new insight for therapy of CRC that GA reduced miR-21 expression and blocked PI3K/Akt to cause HT-29 cancer cell death

-

[105]

miR-196b-5p

Up

Inhibited

in CRC cells, increased the cell cycle, proliferation, invasion, and migration, while reduced cell apoptosis

In vivo

[107]

miR-149

Down

Activated

In CRC), circRNA 100146 is observed overexpressed in both cancer tissues and cells. Experimental results showed that when circRNA 100146 was downregulated in laboratory conditions, it led to several effects: inhibited cell growth, enhanced cell apoptosis, reduced cell migration and invasion, and decelerated tumor growth in live subjects. Moreover, circRNA 100146 acted to inhibit miR-149, which, in turn, regulated and limited the expression of HMGA2

In vivo/in vitro

[108]

miR-338-3p

Down

Inhibited

Knockdown increased cell proliferation and migration while suppressing G1/S cell cycle arrest and death

In vitro

[109]

miR-4260

Up

Down

Cell growth and movement were increased, but apoptosis was reduced

In vivo

[110]

miR-296

Up

Activated

as a result of which cell development was reduced and cell apoptosis was raised

-

[111]

miR-4262

Up

Activated

Lowering the expression of miR-4262 in CRC cells led to a reduction in cell growth and an increase in cell mortality. Conversely, when CRC cells were introduced to the antisense of miR-4262 (as-miR-4262), cell growth increased, and the occurrence of apoptosis decreased

In vivo

[112]

miR-34a/449a

Up

Activated

Reduced miR-34a/449a cluster levels resulted in reduced CRC cell growth and survival, as well as an increase in CRC cell death. This was accomplished by specifically targeting and reducing CASP3 expression via particular locations in the 3'-untranslated region (3'-UTR) of CASP3 mRNA

In vivo

[114]

miR-421

Down

Activated

Reduced miR-34a/449a cluster levels resulted in reduced the rate of the CRC cell growth and survival, as well as an increase in CRC cell death. This was accomplished by specifically targeting and reducing CASP3 expression

In vitro

[115]

miR-1301

Up

Activated

In vitro and in vivo, it decreased cell proliferative growth, invasion, and enhanced the rate of cell death and apoptosis by inhibiting Cyclin A1, PCNA, N-cadherin, and Bcl-2 expression while boosting E-cadherin and Bax expression

In vivo/ in vitro

[126]

miR-133A

Up

Activated

In human CRC, upregulating cell proliferation, movement, migration, and apoptosis by targeting SOX9

In vitro

[287]

LncRNAs

lncRNA AC125257.1

Up

Inhibited

* inhibited tumor growth in vivo and inhibited CRC progression in vitro

* inhibited CASC5's pathogenic overexpression

* inhibited the development of CRC via the miR-873-5p/CASC5 axis

In vivo / iv in vitro

[288]

long non-coding RNA HAND2 antisense RNA 1 (HAND2-AS1)

Up

Activated

inhibited CRC cell line migration and proliferation

In vivo

[289]

LINC00963-v2/-v3

Up

Activated

inhibited migration, viability, and cell proliferation

In vitro

[290]

lncRNA-MALAT1

Down

Activated

* can potentially reduce colony survival, reproduction, and migration

*enhanced G2/M phase arrest, apoptosis, and the development of gamma-H2AX foci in HCT116

In vivo

[291]

Lnc-S100B-2

Down

Activated

CRC cells' capacity for proliferation decreased

In vivo

[119]

lncRNA-ABHD11-AS1

Down

Activated

CRC cell migration, proliferative growth, and invasion were all reduced

In vitro / in vivo

[292]

lnc-TLCD2-1

Up

Inhibited

Compared to the negative control group, the number of cell colonies dramatically increased, and cell apoptosis decreased. Unlike HCT116, CCL244 cell colonies and apoptosis showed impaired lnc-TLCD2-1 expression

In vitro

[293]

lncRNA-PVT1

Down

Activated

As a result of decreased expression of Akt and presumed phosphatidylinositol 3-kinase (PI3K), cell death was enhanced and cell proliferation and invasion were repressed

In vitro

[294]

lncRNA RUNX1-IT1

Down

Activated

regulating cell migration, cell death(apoptosis), and cell proliferation

In vitro

[295]

lncRNA TCF7

Down

no effect on apoptosis

lncTCF7 may act as a possible prognostic indicator, aid in the progression and spread of CRC, and so emerge as a novel diagnostic tool and therapeutic target in CRC therapy

In vitro

[296]

lncRNA lnc-sox5

Up

no effect on apoptosis

elevated rates of CRC. Although lnc-sox5 knockdown did not affect CRC cell growth, cell cycle, or cell apoptosis, it did suppress CRC cell migration and invasion

In vivo

[297]

LINC00174

Up

Inhibited

In vitro studies using LINC00174 showed that it was essential for promoting CRC cell migration, invasion, apoptosis resistance, and cell proliferation

In vitro

[298]

lncRNA FALEC

Down

activated

Inhibiting ALEC caused gastric cancer (GC) cells to stop proliferating, migrating, and invading while simultaneously facilitated apoptosis and autophagy in cultured cells

In vitro

[299]

RP11-468E2.5

Up

Activated

The JAK/STAT signaling pathway is hampered by concentrating on STAT5 and STAT6, which ultimately reduces cell proliferation and increases cell apoptosis in CRC

In vivo

[116]

BANCR

Down

Activated

Inhibited cell proliferation and invasion abilities, raised the rate of apoptosis, and heightened cell sensitivity to ADR (Adriamycin)

In vivo

[118]

LncRNA DANCR

Up

Inhibited

Enhanced the expression of the oncogenic lncRNA MALAT1 by facilitating the stability of MALAT1 RNA, consequently inhibiting apoptosis

In vivo / in vitro

[120]

lncRNA MALAT1

Up

Inhibited

Effectively facilitated DANCR's inhibitory role in apoptosis

In vivo / in vitro

[120]

GAS5

Up

Activated

could prevent the growth and proliferating of cells

In vivo / in vitro

[122]

BLACAT1

Down

Activated

restricted invasion, migration, and proliferation

In vivo

[123]

CRLM

Up

Inhibited

correlated with the expression of pro-metastatic genes controlled by CRLM1 and were associated with chromatin regions of genes related to DNA damage and cell adhesion

In vivo / in vitro

[124]

RPLP0P2

Up

Inhibited

RPLP0P2 facilitated CRC cell proliferation, invasion, and migration while preventing apoptosis (an oncogene in CRC)

In vitro

[124]

RNCR3

Down

Activated

In vitro and in vivo, it decreased cell proleferative growth, invasion, and enhanced apoptosis by limiting Cyclin A1, PCNA, N-cadherin, and Bcl-2 expression while boosting E-cadherin and Bax expression

In vivo / in vitro

[126]

LINC00460

Down

Activated

CRC cell growth was slowed

In vivo / in vitro

[127]

lncRNA RMST

Up

Activated

Cell proliferation and colony formation are inhibited

In vitro

[128]

Long Non-Coding RNA Duxap8

Down

Activated

CRC cells' growth was suppressed and apoptosis was promoted

In vivo/in vitro

[130]

HCG11

Down

Activated

Cell growth, migration, and invasion were all inhibited

In vitro

[129]

circRNAs

Circ_0087862

Down

Activated

Cell growth, invasion, and glycolysis were all inhibited

In vivo

[261]

circ_0004585

Down

Activated

*Circ_0004585's silencing prevented angiogenesis, EMT, proliferation, the growth of the tumor, and death(apoptosis) in CRC cells

In vivo

[263]

Circ_FMN2

Up

Inhibited

encourage CRC cell growth, metastasis, and tumor development

In vivo

[300]

Circ_0005615

Up

Activated

influenced the development of CRC cancer by regulating FOSL2 expression and sponging miR-873-5p

In vivo

[301]

si-circPDE4D

Up

Inhibited

encouraged cell migration, proliferation, and invasion

In vitro

[302]

circ_0084188

Down

Inhibited

*inhibited CRC cell movement, proliferative growth, and invasion

In vivo

[272]

circRNA_0001658 (circ_0001658)

Up

Inhibited

accelerated the cell cycle and enhanced HT29 cell proliferation

In vitro / in vivo

[303]

circSETD3

Up

Activated

CircSETD3 directly sponged miR-653 and controls miR-653 negatively to influence CRC cell proliferation, migration, invasion, and apoptosis

In vitro

[275]

circ_0082182

Down

Activated

Slowed down OXA invasion, migratory, proliferative, and resistance

In vivo

[304]

circ-CD44

Down

Activated

OXA sensitivity was raised whereas proliferative growth, migration, and invasion were limited

In vivo

[305]

circ_0067717

Down

Activated

restricted invasion, proliferation, and glutamine metabolism of CRC cells

In vivo

[306]

Circ_0011385

Down

Activated

inhibited invasion, migration, and cell proliferation

In vivo

[307]

Circ_0003602

Down

Activated

reduced migration, invasion, angiogenesis, and glutaminolysis of CRC cells

Iv vivo

[308]

hsa_circ_0057104 (circPDK1)

Down

Activated

*Reduced forced apoptosis, warburg effect, invasion/migration, and CRC proliferative cell growth

*CCND2 expression was mediated by CircPDK1 through miR-627-5p'scompetitiveadsorption

In vitro

[136]

circPGPEP1

Down

Activated

In addition to successfully limiting CRC immune escape, EMT, migration, and cell proliferation and accelerating apoptosis in vitro, circPGPEP1 knockdown also prevented the advancement of CRC tumors and immunological escape in vivo

In vivo

[309]

circRNA 100146

Down

Activated

inhibited tumor development in vivo, decreased migration and invasion, increased apoptosis, and suppressed cell proliferation in vitro

In vitro / in vivo

[108]

Circ_0058123

Down

Activated

enhanced cell death while suppressing CRC cell proliferation, migration, invasion, and tube formation

In vivo

[137]

Circ_0000370

Down

Activated

caused cell death but decreased CRC cell growth, migration, and invasion

In vivo

[138]

Circ_0000395

Up

Activated

accelerated CRC cell apoptosis, prevented CRC invasion, migration, cell proliferation, and EMT in vitro, and slowed down CRC growth and progression in mice models in vivo

In vitro / in vivo

[139]

circ_0001821

Down

Activated

decreased ability of cells to proliferate, migrate, invade, and use glycolysis

In vivo

[140]

Circ_0004585

Down

Activated

impeded colony formation, cell migration, and invasion, as well as CRC cell viability

In vivo

[141]

Circ_0001535

Down

Activated

prevented cell migration, invasion, and angiogenesis

In vivo

[142]

Circ_0101802

Down

Activated

restricted tube formation, proliferative growth, and migration

In vivo

[194]

circ_0000467

Down

Activated

impeded invasion, glycolysis, proliferative growth, and migration

In vitro / in vivo

[143]

circ_0068464

Down

Activated

knockdown the expression of proteins associated with the Wnt/-catenin pathway and limited CRC cell motility and proliferation

In vitro / in vivo

[310]

Circ_0001535

Down

Activated

inhibited CRC cells from exhibiting malignant and oncogenic traits such as proliferation, invasion, and tumor development

In vivo

[144]

circ_PTPRA

Up

Activated

CRC tissue and cell cycle arrest was enhanced, and cell growth was silenced. moreover, exosomal circ_PTPRA increased the radio-sensitivity of CRC cells

In vivo

[311]

Circ_0007031

Down

Activated

inhibited cell growth, whereas it caused cell arrest at the G0/G1 phase

In vivo

[312]

circRAD23B

Down

Activated

slowed down CRC cell growth, cell cycle progression, and cell metastasis

In vivo

[145]

hsa_circ_0000523

Up

Activated

decreased the growth of SW480 and SW620 cells

In vitro

[131]

CircLMNB1

Down

Activated

reduced cell migration, invasion, and proliferation while increasing cell cycle arrest

In vitro

[132]

circCUL2

Up

Activated

decreased the ability of CRC cells to proliferate and instead brought on apoptosis and autophagy

In vivo

[133]

circular ZFR (circZFR)

Down

Activated

increased cell cycle arrest in the G1/S phase, and decreased growth

In vitro

[313]

circ_0001666

Up

Activated

limited cell invasion and proliferation while decreasing the number of CD133 + cells

In Vitro / In Vivo

[314]